Abstract 5127: Reprogramming of EMT and stemness by human recombinant CCN5 in triple negative breast cancer cells

• Published in: Cancer research (Chicago, Ill.) Vol. 74; no. 19_Supplement; p. 5127
• Main Authors: Das, Amlan, De, Archana, Banerjee, Snigdha, Banerjee, Sushanta K.
• Format: Journal Article
• Language: English
• Published: 01-10-2014
• ISSN: 0008-5472; 1538-7445
• DOI: 10.1158/1538-7445.AM2014-5127

Abstract
Epithelial to Mesenchymal transition (EMT) is an important and coordinated series of events associated with tumor metastasis and invasion. Recent studies from our group had shown the importance of CCN5/ WISP-2 in the suppression of breast and pancreatic cancer progression through the regulation of the invasive phenotypes. In our study we have observed that exposure of triple negative human breast cancer cells (TNBC), MDA-MB-231 and HCC-70 to recombinant CCN5 (hrCCN5), resulted in a dose-dependent inhibition of cell-proliferation through the induction of apoptotic cell death. Anchorage-independent growth and colony forming ability of MDA-MB-231 cells were also found to be drastically inhibited in the presence of hrCCN5. Distinct up regulation of the epithelial markers such as CD24, and cytokeratin19 and down regulation of the mesenchymal markers such as Notch-1, vimentin, and CD44 were observed in CCN5 treated TNBC cells. CCN5 treatment also resulted in the significant reduction of stemness of these cells, as confirmed by mammosphere assay. Collectively, the studies indicate CCN5 could be a re-programmer of EMT and stemness and thus hrCCN5 can be considered as a potential therapeutic agent for TNBC.
Note: This abstract was not presented at the meeting.
Citation Format: Amlan Das, Archana De, Snigdha Banerjee, Sushanta K. Banerjee. Reprogramming of EMT and stemness by human recombinant CCN5 in triple negative breast cancer cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 5127. doi:10.1158/1538-7445.AM2014-5127