IQUIFIB 02644
INSTITUTO DE QUIMICA Y FISICOQUIMICA BIOLOGICAS "PROF. ALEJANDRO C. PALADINI"
Unidad Ejecutora - UE
artículos
Título:
Apoptotic effect of a chimeric interferon-alpha2b peptide
Autor/es:
BLANK, V. C; PEÑA, C; ROGUIN, L. P
Revista:
Cancer Biology and Therapy
Editorial:
Landes Bioscience
Referencias:
Lugar: Texas, USA; Año: 2007 vol. 6 p. 1787 - 1793
ISSN:
1538-4047
Resumen:
Interferons alpha (IFNsa) are a family of related proteins exhibiting antiviral,
antiproliferative and immunoregulatory activities. Although IFNsa have been widely
employed for the pharmacological treatment of different types of cancer, the therapeutic
efficacy occasionally can be diminished by the appearance of side effects, neutralizing
antibodies or tumor resistance. In the search of mimetic peptides of the IFN‑a2b molecule,
we have recently synthesized a chimeric cyclic peptide that inhibits IFN‑a2b binding to its
receptor and exerts an IFN‑like antiproliferative activity. In order to study the mechanism
of growth inhibition of the cyclic chimera, we evaluated its ability to induce cell cycle
arrest or apoptosis in WISH cells. We found that the chimeric peptide did not cause a cell
cycle arrest, although the entire IFN‑a2b molecule did modify cell cycle by increasing the
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
receptor and exerts an IFN‑like antiproliferative activity. In order to study the mechanism
of growth inhibition of the cyclic chimera, we evaluated its ability to induce cell cycle
arrest or apoptosis in WISH cells. We found that the chimeric peptide did not cause a cell
cycle arrest, although the entire IFN‑a2b molecule did modify cell cycle by increasing the
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
we have recently synthesized a chimeric cyclic peptide that inhibits IFN‑a2b binding to its
receptor and exerts an IFN‑like antiproliferative activity. In order to study the mechanism
of growth inhibition of the cyclic chimera, we evaluated its ability to induce cell cycle
arrest or apoptosis in WISH cells. We found that the chimeric peptide did not cause a cell
cycle arrest, although the entire IFN‑a2b molecule did modify cell cycle by increasing the
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
receptor and exerts an IFN‑like antiproliferative activity. In order to study the mechanism
of growth inhibition of the cyclic chimera, we evaluated its ability to induce cell cycle
arrest or apoptosis in WISH cells. We found that the chimeric peptide did not cause a cell
cycle arrest, although the entire IFN‑a2b molecule did modify cell cycle by increasing the
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
employed for the pharmacological treatment of different types of cancer, the therapeutic
efficacy occasionally can be diminished by the appearance of side effects, neutralizing
antibodies or tumor resistance. In the search of mimetic peptides of the IFN‑a2b molecule,
we have recently synthesized a chimeric cyclic peptide that inhibits IFN‑a2b binding to its
receptor and exerts an IFN‑like antiproliferative activity. In order to study the mechanism
of growth inhibition of the cyclic chimera, we evaluated its ability to induce cell cycle
arrest or apoptosis in WISH cells. We found that the chimeric peptide did not cause a cell
cycle arrest, although the entire IFN‑a2b molecule did modify cell cycle by increasing the
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
receptor and exerts an IFN‑like antiproliferative activity. In order to study the mechanism
of growth inhibition of the cyclic chimera, we evaluated its ability to induce cell cycle
arrest or apoptosis in WISH cells. We found that the chimeric peptide did not cause a cell
cycle arrest, although the entire IFN‑a2b molecule did modify cell cycle by increasing the
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
we have recently synthesized a chimeric cyclic peptide that inhibits IFN‑a2b binding to its
receptor and exerts an IFN‑like antiproliferative activity. In order to study the mechanism
of growth inhibition of the cyclic chimera, we evaluated its ability to induce cell cycle
arrest or apoptosis in WISH cells. We found that the chimeric peptide did not cause a cell
cycle arrest, although the entire IFN‑a2b molecule did modify cell cycle by increasing the
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
receptor and exerts an IFN‑like antiproliferative activity. In order to study the mechanism
of growth inhibition of the cyclic chimera, we evaluated its ability to induce cell cycle
arrest or apoptosis in WISH cells. We found that the chimeric peptide did not cause a cell
cycle arrest, although the entire IFN‑a2b molecule did modify cell cycle by increasing the
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
antiproliferative and immunoregulatory activities. Although IFNsa have been widely
employed for the pharmacological treatment of different types of cancer, the therapeutic
efficacy occasionally can be diminished by the appearance of side effects, neutralizing
antibodies or tumor resistance. In the search of mimetic peptides of the IFN‑a2b molecule,
we have recently synthesized a chimeric cyclic peptide that inhibits IFN‑a2b binding to its
receptor and exerts an IFN‑like antiproliferative activity. In order to study the mechanism
of growth inhibition of the cyclic chimera, we evaluated its ability to induce cell cycle
arrest or apoptosis in WISH cells. We found that the chimeric peptide did not cause a cell
cycle arrest, although the entire IFN‑a2b molecule did modify cell cycle by increasing the
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
receptor and exerts an IFN‑like antiproliferative activity. In order to study the mechanism
of growth inhibition of the cyclic chimera, we evaluated its ability to induce cell cycle
arrest or apoptosis in WISH cells. We found that the chimeric peptide did not cause a cell
cycle arrest, although the entire IFN‑a2b molecule did modify cell cycle by increasing the
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
we have recently synthesized a chimeric cyclic peptide that inhibits IFN‑a2b binding to its
receptor and exerts an IFN‑like antiproliferative activity. In order to study the mechanism
of growth inhibition of the cyclic chimera, we evaluated its ability to induce cell cycle
arrest or apoptosis in WISH cells. We found that the chimeric peptide did not cause a cell
cycle arrest, although the entire IFN‑a2b molecule did modify cell cycle by increasing the
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
receptor and exerts an IFN‑like antiproliferative activity. In order to study the mechanism
of growth inhibition of the cyclic chimera, we evaluated its ability to induce cell cycle
arrest or apoptosis in WISH cells. We found that the chimeric peptide did not cause a cell
cycle arrest, although the entire IFN‑a2b molecule did modify cell cycle by increasing the
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
employed for the pharmacological treatment of different types of cancer, the therapeutic
efficacy occasionally can be diminished by the appearance of side effects, neutralizing
antibodies or tumor resistance. In the search of mimetic peptides of the IFN‑a2b molecule,
we have recently synthesized a chimeric cyclic peptide that inhibits IFN‑a2b binding to its
receptor and exerts an IFN‑like antiproliferative activity. In order to study the mechanism
of growth inhibition of the cyclic chimera, we evaluated its ability to induce cell cycle
arrest or apoptosis in WISH cells. We found that the chimeric peptide did not cause a cell
cycle arrest, although the entire IFN‑a2b molecule did modify cell cycle by increasing the
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
receptor and exerts an IFN‑like antiproliferative activity. In order to study the mechanism
of growth inhibition of the cyclic chimera, we evaluated its ability to induce cell cycle
arrest or apoptosis in WISH cells. We found that the chimeric peptide did not cause a cell
cycle arrest, although the entire IFN‑a2b molecule did modify cell cycle by increasing the
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
we have recently synthesized a chimeric cyclic peptide that inhibits IFN‑a2b binding to its
receptor and exerts an IFN‑like antiproliferative activity. In order to study the mechanism
of growth inhibition of the cyclic chimera, we evaluated its ability to induce cell cycle
arrest or apoptosis in WISH cells. We found that the chimeric peptide did not cause a cell
cycle arrest, although the entire IFN‑a2b molecule did modify cell cycle by increasing the
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
receptor and exerts an IFN‑like antiproliferative activity. In order to study the mechanism
of growth inhibition of the cyclic chimera, we evaluated its ability to induce cell cycle
arrest or apoptosis in WISH cells. We found that the chimeric peptide did not cause a cell
cycle arrest, although the entire IFN‑a2b molecule did modify cell cycle by increasing the
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
number of S‑phase cells. In spite of this difference, both molecules were able to induce
apoptosis through the activation of caspases 8 and 9, indicating the involvement of death
receptor and mitochondrial pathways. In addition, both peptidic derivative and IFN‑a2b
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
altered the expression of Bcl‑2 family proteins and induced the release of cytochrome
C to cytosol, supporting the participation of mitochondrial pathway in the induction of
apoptosis. In conclusion, we demonstrated that the chimeric cyclic peptide behaved as
a potent inducer of apoptosis and it could be a potentially useful agent for the treatment
of certain malignancies.
