E2F6 functions as a competing endogenous RNA, and transcriptional repressor, to promote ovarian cancer stemness.

ABSTRACT: Ovarian cancer is the most lethal cancer of the female reproductive system. In that regard, several epidemiological studies suggest that long-term exposure to estrogen could increase ovarian cancer risk, although its precise role remains controversial. To decipher a mechanism for this, we previously generated a mathematical model of how estrogen-mediated upregulation of the transcription factor, E2F6, upregulates the ovarian cancer stem/initiating cell marker, c-Kit, by epigenetic silencing the tumor suppressor miR-193a, and a competing endogenous (ceRNA) mechanism. In this study, we tested that previous mathematical model, showing that estrogen treatment of immortalized ovarian surface epithelial cells upregulated both E2F6 and c-KIT, but downregulated miR-193a. Luciferase assays further

SUBMITTER: Cheng FHC 

PROVIDER: S-EPMC6398890 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature