Loss of calponin h1 confers anoikis resistance and tumor progression in the development of high-grade serous carcinoma originating from the fallopian tube epithelium.

ABSTRACT: Increasing evidence indicates that ovarian high-grade serous carcinoma (HGSC) originates from the fallopian tube epithelium and metastasizes to the ovary as the secondary site. A working hypothesis is that detached tubal HGSC cells survive anoikis and implant on the ovary. In this study, we found that downregulation of calponin h1 (CNN1) is necessary for the anoikis survival and cell transformation. CNN1 was progressively downregulated in cells and tissues representing different stages of HGSC development from fallopian tube epithelium (FTE). Knock down of CNN1 in immortalized human FTE cells conferred gains of resistance to anoikis and transformation phenotypes including anchorage independent growth (AIG) and xenograft tumorigenesis in NSG mice. Conversely, overexpression of CNN1 in RAS-t

SUBMITTER: Wang KH 

PROVIDER: S-EPMC5617412 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature