INVESTIGADORES
URTREGER Alejandro Jorge
artículos
Título:
Modulation of pancreatic tumor potential by overexpression protein kinase C beta1 (PKCb1)
Autor/es:
STÉFANO M. CIRIGLIANO; LAURA V. MAURO; VALERIA C. GROSSONI; LUCAS L. COLOMBO; MIRIAM J. DIAMENT; MARCELO G. KAZANIETZ; ELISA D. BAL DE KIER JOFFÉ; LYDIA I. PURICELLI; ALEJANDRO J. URTREGER
Revista:
PANCREAS.
Editorial:
LIPPINCOTT WILLIAMS & WILKINS
Referencias:
Lugar: Hagerstown; Año: 2013 vol. 42 p. 1060 - 1069
ISSN:
0885-3177
Resumen:
Objective: to investigate whether the overexpression of PKCb1 is able to modulate the malignant phenotype displayed by the human ductal pancreatic carcinoma cell line PANC1. Methods: PKCb1 overexpression was achieved using a stable transfection approach. PANC1-PKCb1 and control cells were analyzed both in vitro and in vivo. Results: PANC1-PKCb1 cells displayed a lower growth capacity associated with the downregulation of the MEK/ERK pathway and cyclin expression. Furthermore, PKCb1 overexpression was associated with an enhancement of cell adhesion to fibronectin and with reduced migratory and invasive phenotypes. In agreement with these results, PANC1-PKCb1 cells showed an impaired ability to secrete proteolytic enzymes. We also found that PKCb1 overexpressing cells were more resistant to cell death induced by serum deprivation, an event associated with G0/G1 arrest and the modulation of PI3K/Akt and NF-kB pathways. Most notably, the overexpression of PKCb1 completely abolished the ability of PANC1 cells to induce tumors in nude mice. Conclusions: our results established an important role for PKCb1 in PANC1 cells suggesting it would act as a suppressor of tumorigenic behavior in pancreatic cancer.