RGS16, a novel p53 and pRb cross-talk candidate inhibits migration and invasion of pancreatic cancer cells
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https://doi.org/10.18632/genesandcancer.43
Miranda B. Carper1,2, James Denvir2, Goran Boskovic2, Donald A. Primerano2 and Pier Paolo Claudio1,2,3
1 McKown Translational Genomic Research Institute, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV, USA
2 Department of Biochemistry and Microbiology, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV, USA
3 Department of Surgery, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV, USA
Correspondence:
Pier Paolo Claudio, email:
Keywords: p53, pRb, RGS16, EGF, migration, pancreatic cancer
Received: October 8, 2014 Accepted: November 26, 2014 Published: November 27, 2014
Abstract
Data collected since the discovery of p53 and pRb/RB1 suggests these tumor suppressors cooperate to inhibit tumor progression. Patients who have mutations in both p53 and RB1 genes have increased tumor reoccurrence and decreased survival compared to patients with only one tumor suppressor gene inactivated. It remains unclear how p53 and pRb cooperate toward inhibiting tumorigenesis. Using RNA expression profiling we identified 179 p53 and pRb cross-talk candidates in normal lung fibroblasts (WI38) cells exogenously coexpressing p53 and pRb. Regulator of G protein signaling 16 (RGS16) was among the p53 and pRb cross-talk candidates and has been implicated in inhibiting activation of several oncogenic pathways associated with proliferation, migration, and invasion of cancer cells.
RGS16 has been found to be downregulated in pancreatic cancer patients with metastases compared to patients without metastasis. Expression of RGS16 mRNA was decreased in the pancreatic cancer cell lines tested compared to control. Expression of RGS16 inhibited migration of the BxPC-3 and AsPC-1 but not PANC-1 cells and inhibited invasion of BxPC-3 and AsPC-1 cells with no impact on cell viability. We have identified for the first time p53 and pRb cross-talk candidates and a role for RGS16 to inhibit pancreatic cancer migration and invasion.
