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 ,
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.
