| General information | Literature | Expression | Regulation | Mutation | Interaction |
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Basic Information |
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|---|---|
Gene ID | 5579 |
Name | PRKCB |
Synonymous | PKC-beta|PKCB|PRKCB1|PRKCB2;protein kinase C, beta;PRKCB;protein kinase C, beta |
Definition | PKC-B|protein kinase C beta type|protein kinase C, beta 1 polypeptide |
Position | 16p11.2 |
Gene type | protein-coding |
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Title |
Abstract |
| Modulation of pancreatic tumor potential by overexpression of protein kinase C beta1. | OBJECTIVE: This study aimed to investigate whether the overexpression of protein kinase C beta1 (PKCbeta1) is able to modulate the malignant phenotype displayed by the human ductal pancreatic carcinoma cell line PANC1. METHODS: PKCbeta1 overexpression was achieved using a stable transfection approach. PANC1-PKCbeta1 and control cells were analyzed both in vitro and in vivo. RESULTS: PANC1-PKCbeta1 cells displayed a lower growth capacity associated with the down-regulation of the MEK/ERK pathway and cyclin expression. Furthermore, PKCbeta1 overexpression was associated with an enhancement of cell adhesion to fibronectin and with reduced migratory and invasive phenotypes. In agreement with these results, PANC1-PKCbeta1 cells showed an impaired ability to secrete proteolytic enzymes. We also found that PKCbeta1 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-kappaB pathways. Most notably, the overexpression of PKCbeta1 completely abolished the ability of PANC1 cells to induce tumors in nude mice. CONCLUSIONS: Our results established an important role for PKCbeta1 in PANC1 cells suggesting it would act as a suppressor of tumorigenic behavior in pancreatic cancer. |