Open AccessSonic advance: CCN1 regulates sonic hedgehog in pancreatic cancer
Author(s) -
Leask Andrew
Publication year - 2013
Publication title -
journal of cell communication and signaling
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 44
eISSN - 1873-961X
pISSN - 1873-9601
DOI - 10.1007/s12079-012-0187-x
Subject(s) - sonic hedgehog , pancreatic cancer , cancer research , matricellular protein , metastasis , hedgehog , cancer , epithelial–mesenchymal transition , cyr61 , tumor microenvironment , cancer cell , biology , microbiology and biotechnology , medicine , ctgf , signal transduction , extracellular matrix , growth factor , receptor , tumor cells
Pancreatic ductal adenocarcinoma (PDAC) is the fifth leading cause of cancer internationally. As the precise molecular pathways that regulate pancreatic cancer are incompletely understood, appropriate targets for drug intervention remain elusive. It is being increasingly appreciated that the cellular microenvironment plays an important role in driving tumor growth and metastasis. CCN1, a member of the CCN family of secreted matricellular proteins, is overexpressed in pancreatic cancer, and may represent a novel target for therapy. Sonic hedgehog (SHh) is responsible for PDAC cell proliferation, epithelial‐mesenchymal transition (EMT), maintenance of cancer stemness, migration, invasion, and metastatic growth; in a recent report, it was shown that CCN1 is a potent regulator of SHh expression via Notch‐1. CCN1 activity was mediated, at least in part, through altering proteosome activity. These results suggest that CCN1 may be an ideal target for treating PDAC.