IBIMOL   23987
INSTITUTO DE BIOQUIMICA Y MEDICINA MOLECULAR PROFESOR ALBERTO BOVERIS
Unidad Ejecutora - UE
artículos
Título:
Curcumin induces cell-arrest and apoptosis in association with the inhibition of
Autor/es:
G. G. MACKENZIE; N. QUEISSER; M. L. WOLFSON; C. G. FRAGA; A. M. ADAMO; P. I. OTEIZA
Revista:
INTERNATIONAL JOURNAL OF CANCER. JOURNAL INTERNATIONAL DU CANCER.
Editorial:
Wiley-Liss
Referencias:
Año: 2008 vol. 123 p. 56 - 65
ISSN:
0020-7136
Resumen:
Although treatment of Hodgkins lymphoma (HL) with a multidrug
approach has been very successful, its toxicity becomes evident
after several years as secondary malignancies and cardiovascular
disease. Therefore, the current goal in HL treatment is to
find new therapies that specifically target the deregulated signaling
cascades, such as NF-jB and STAT3, which cause Hodgkin
and Reed-Sternberg (H-RS) cell proliferation and resistance of apoptosis.
Based on the above information, we investigated the
capacity of curcumin to inhibit NF-jB and STAT3 in H-RS cells,
characterizing the functional consequences. Curcumin is incorporated
into H-RS cells and acts inhibiting both NF-jB and STAT3
activation, leading to a decreased expression of proteins involved
in cell proliferation and apoptosis, e.g. Bcl-2, Bcl-xL, cFLIP,
XIAP, c-IAP1, survivin, c-myc and cyclin D1. Interestingly, curcumin
caused cell cycle arrest in G2-M and a significant reduction
(8097%) in H-RS cell viability. Furthermore, curcumin triggered
cell death by apoptosis, as evidenced by the activation of caspase-3
and caspase-9, changes in nuclear morphology and phosphatidylserine
translocation. The above findings provide a mechanistic rationale
for the potential use of curcumin as a therapeutic agent for
patients with HL.jB and STAT3, which cause Hodgkin
and Reed-Sternberg (H-RS) cell proliferation and resistance of apoptosis.
Based on the above information, we investigated the
capacity of curcumin to inhibit NF-jB and STAT3 in H-RS cells,
characterizing the functional consequences. Curcumin is incorporated
into H-RS cells and acts inhibiting both NF-jB and STAT3
activation, leading to a decreased expression of proteins involved
in cell proliferation and apoptosis, e.g. Bcl-2, Bcl-xL, cFLIP,
XIAP, c-IAP1, survivin, c-myc and cyclin D1. Interestingly, curcumin
caused cell cycle arrest in G2-M and a significant reduction
(8097%) in H-RS cell viability. Furthermore, curcumin triggered
cell death by apoptosis, as evidenced by the activation of caspase-3
and caspase-9, changes in nuclear morphology and phosphatidylserine
translocation. The above findings provide a mechanistic rationale
for the potential use of curcumin as a therapeutic agent for
patients with HL.jB and STAT3 in H-RS cells,
characterizing the functional consequences. Curcumin is incorporated
into H-RS cells and acts inhibiting both NF-jB and STAT3
activation, leading to a decreased expression of proteins involved
in cell proliferation and apoptosis, e.g. Bcl-2, Bcl-xL, cFLIP,
XIAP, c-IAP1, survivin, c-myc and cyclin D1. Interestingly, curcumin
caused cell cycle arrest in G2-M and a significant reduction
(8097%) in H-RS cell viability. Furthermore, curcumin triggered
cell death by apoptosis, as evidenced by the activation of caspase-3
and caspase-9, changes in nuclear morphology and phosphatidylserine
translocation. The above findings provide a mechanistic rationale
for the potential use of curcumin as a therapeutic agent for
patients with HL.jB and STAT3
activation, leading to a decreased expression of proteins involved
in cell proliferation and apoptosis, e.g. Bcl-2, Bcl-xL, cFLIP,
XIAP, c-IAP1, survivin, c-myc and cyclin D1. Interestingly, curcumin
caused cell cycle arrest in G2-M and a significant reduction
(8097%) in H-RS cell viability. Furthermore, curcumin triggered
cell death by apoptosis, as evidenced by the activation of caspase-3
and caspase-9, changes in nuclear morphology and phosphatidylserine
translocation. The above findings provide a mechanistic rationale
for the potential use of curcumin as a therapeutic agent for
patients with HL.e.g. Bcl-2, Bcl-xL, cFLIP,
XIAP, c-IAP1, survivin, c-myc and cyclin D1. Interestingly, curcumin
caused cell cycle arrest in G2-M and a significant reduction
(8097%) in H-RS cell viability. Furthermore, curcumin triggered
cell death by apoptosis, as evidenced by the activation of caspase-3
and caspase-9, changes in nuclear morphology and phosphatidylserine
translocation. The above findings provide a mechanistic rationale
for the potential use of curcumin as a therapeutic agent for
patients with HL.