Title of article
Loss of WISP-2/CCN5 signaling in human pancreatic cancer: A potential mechanism for epithelial-mesenchymal-transition
Author/Authors
Dhar، نويسنده , , Gopal and Mehta، نويسنده , , Smita and Banerjee، نويسنده , , Snigdha and Gardner، نويسنده , , Ashleigh and McCarty، نويسنده , , Bryan M. and Mathur، نويسنده , , Sharad C. and Campbell، نويسنده , , Donald R. and Kambhampati، نويسنده , , Suman and Banerjee، نويسنده , , Sushanta K.، نويسنده ,
Issue Information
روزنامه با شماره پیاپی سال 2007
Pages
8
From page
63
To page
70
Abstract
The objective of this study was to explore the pathophysiological relevance of WISP-2/CCN5 in progression of human pancreatic adenocarcinoma (PAC). We found WISP-2/CCN5 mRNA and protein expression was faint and sporadic in PAC and detected in only 8.7–20% of the samples with varying grades as compared to adjacent normal and chronic pancreatitis samples where expression was very high in the ducts and acini. Colocalization studies in tissue-microarray slides revealed WISP-2/CCN5 mRNA loss was associated with p53 overexpression in PAC. Like tissue samples, p53 mutant-PAC cell lines show loss of WISP-2/CCN5. Moreover, functional analysis studies demonstrate exposure of pancreatic cancer cells to WISP-2/CCN5 recombinant protein enhances mesenchymal–epithelial-transition (MET). Collectively, we suggest WISP-2/CCN5 silencing may be a critical event during differentiation and progression of PAC and mutant p53 is possibly an important player in pursuing this episode.
Keywords
Pancreatic adenocarcinoma , WISP-2/CCN5 , p53 tumor suppressor gene
Journal title
Cancer Letters
Serial Year
2007
Journal title
Cancer Letters
Record number
1810627
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