Abstract:
:MUC16/CA125 is over-expressed in human epithelial tumors including ovarian, breast and some other carcinomas. The purpose of this study is to investigate how cell surface MUC16 is functionally involved in tumor progression, with a special focus on the role of its cytoplasmic tail. Forced expression of C-terminal MUC16 fragment (MUC16C) in epithelial cancer cells increased cell migration. We found that MUC16C directly interacted with Src family kinases (SFKs). Notably, localizations of E-cadherin and β-catenin at the cell-cell contacts were more diffuse in MUC16C transfectants compared with mock transfectants. Furthermore, MUC16C transfectants showed reduced Ca(2+)-dependent cell-cell adhesion, but the treatment of cells with PP2, a SFKs inhibitor, restored this. Because cell surface MUC16 is also associated with the E-cadherin/β-catenin complex, the over-expression of MUC16 and its interaction with SFKs may enhance SFKs-induced deregulation of E-cadherin. Thus, our results suggest a role for cell surface MUC16 in cell-cell adhesion of epithelial cancer cells.
journal_name
Eur J Cell Bioljournal_title
European journal of cell biologyauthors
Akita K,Tanaka M,Tanida S,Mori Y,Toda M,Nakada Hdoi
10.1016/j.ejcb.2013.10.005subject
Has Abstractpub_date
2013-08-01 00:00:00pages
257-63issue
8-9eissn
0171-9335issn
1618-1298pii
S0171-9335(13)00064-2journal_volume
92pub_type
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