Inhibition of cellular growth and migration by suppression of endothelial protein C receptor (EPCR) in lung carcinoma cells.

Abstract:

:Increasing evidence shows that beyond its role in coagulation, thrombosis interferes with carcinogenesis. Endothelial cell protein C receptor (EPCR) is a cellular receptor for protein C and activated protein C (APC). Such EPCR-induced signal transduction promotes cancer cell migration, invasion, and angiogenesis and inhibits cancer cell apoptosis. However, its role in lung carcinoma biology is yet to be demonstrated. Here, the recombinant EPCR siRNA plasmids were constructed to investigate the effects of inhibition of EPCR on human lung cancer H1299. EPCR siRNA led to inhibition of endogenous EPCR mRNA and protein expression as determined by RT-PCR and Western blotting analysis. EPCR siRNA significantly inhibited cell growth, blocked entry into the S phase of the cell cycle, and reduced the migration of H1299 cells. EPCR siRNA also decreases MMP-2 and cyclin E expression in H1299 cells. In addition, siRNA targeting of EPCR inhibited the growth of H1299 cells and decreased MVD in SCID mice tumor models. Taken together, EPCR was involved in regulating progression of human lung cancer cells. Manipulation of EPCR expression may be a potential therapeutic strategy for lung cancer.

journal_name

Oncol Res

journal_title

Oncology research

authors

Heng W,Huang JA,Wang ZY

doi

10.3727/096504013x13589503482932

subject

Has Abstract

pub_date

2012-01-01 00:00:00

pages

231-40

issue

5-6

eissn

0965-0407

issn

1555-3906

journal_volume

20

pub_type

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