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Investigation of RGS16 mediated inhibition of pancreatic cancer metastasis
Author(s) -
Carper Miranda Bernel,
Boskovic Goran,
Denvir James,
Primerano Donald,
Hardman W. Elaine,
Claudio Pier Paolo
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.611.6
Subject(s) - pancreatic cancer , metastasis , cancer research , biology , cancer , oncogene , cell migration , suppressor , medicine , cell culture , cell cycle , genetics
Pancreatic cancer is ranked as the fourth cause of cancer‐related deaths in the United States with a five‐year survival rate of <5%. This is due in part, to early systemic dissemination. Due to the aggressive nature of this disease, new therapies are needed to inhibit and treat metastatic pancreatic cancer. We have previously performed a microarray analysis to determine proteins regulated by the tumor suppressors p53 and pRb to identify proteins involved in the p53 and pRb cross‐talk pathway. We have found that Regulator of G‐protein signaling (RGS16) is regulated by both p53 and pRb in WI38 normal lung fibroblast cells. RGS16 turns off signaling of several oncogene pathways that are involved in proliferation, chemoresistance, and metastasis. Recently it has also been found that RGS16 is downregulated in metastasized pancreatic cancer. The objective is to investigate the ability of RGS16 to inhibit metastasis by examining pancreatic cancer cell invasion and migration. RGS16 was overexpressed in BxPC‐3 and PANC‐1 pancreatic cancer cell lines. Migration and invasion were investigated using wound‐healing assays and Boyden chambers, respectively. The results suggest that RGS16 is able to inhibit migration and invasion of pancreatic cancer cells. Our data indicates that RGS16 is regulated by both p53 and pRb and overexpression of RGS16 is able to inhibit pancreatic cancer metastasis.