RGS16, a novel p53 and pRb cross-talk candidate inhibits migration and invasion of pancreatic cancer cells.

摘要: Data collected since the discovery of p53 and pRb/RB1 suggests these tumor suppressors cooperate to inhibit progression. Patients who have mutations in both RB1 genes increased reoccurrence decreased survival compared patients with only one suppressor gene inactivated. It remains unclear how pRb toward inhibiting tumorigenesis. Using RNA expression profiling we identified 179 cross-talk candidates normal lung fibroblasts (WI38) cells exogenously coexpressing pRb. Regulator G protein signaling 16 (RGS16) was among has been implicated activation several oncogenic pathways associated proliferation, migration, invasion cancer cells. RGS16 found be downregulated pancreatic metastases without metastasis. Expression RGS16 mRNA cell lines tested control. inhibited migration BxPC-3 AsPC-1 but not PANC-1 no impact on viability. We for first time a role invasion.