Background: Extended from our previously observation that expression of miR-1307 in chemoresistant primary ovarian cancer tissues is elevated, here we are aiming to dissect the function of miR-1307 and its predicted target gene, CIC (capicua transcriptional repressor), in ovarian cancer chemotherapy.
Methods: We evaluated the expression of miR-1307 and CIC in chemoresistant and chemosensitive ovarian cancer tissues and cells by real time-PCR and western blot. We used chemoresistant/chemosensitive cells with miR-1307 suppression/overexpression to study the biological effects of miR-1307 by MTT and flow cytometer. Dual luciferase reporter gene assay was used to validate direct binding between miR-1307 and the 3'-UTR of CIC. Real-time PCR and western blot analyses, MTT and flow cytometry were used to reveal the biological effects of miR-1307 and CIC, as well as their regulation.
Results: We found that miR-1307 affects cell cycle dynamics, cell viability in ovarian cancer cells. In addition, its expression level can influence chemosensitivity to paclitaxel in ovarian cancer cells. We also validate that CIC is a downstream target of miR-1307 via its regulation on 3'-UTR of CIC gene and ETV4 and ETV5 are also regulated by miR-1307/CIC axis.
Conclusions: Our data suggested that miR-1307 may be involved in the resistance of ovarian cancer to chemotherapy drugs via regulation of CIC, and should be further explored as a potential therapeutic target.
Keywords: CIC; Chemoresistant; Chemosensitive; Ovarian cancer; RTK signaling; miR-1307.
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