Long non-coding RNA HOTAIR promotes cervical cancer progression through regulating BCL2 via targeting miR-143-3p.

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Long non-coding RNA HOTAIR promotes cervical cancer progression through regulating BCL2 via targeting miR-143-3p.

Cancer Biol Ther. 2018 Jan 16;:0

Authors: Liu M, Jia J, Wang X, Liu Y, Wang C

Abstract
BACKGROUND: HOX transcript antisense RNA (HOTAIR) is a long non-coding RNA (lncRNA) widely involved in the progression of numerous malignancies. Whereas, the potential molecular mechanism of HOTAIR involved in cervical cancer progression is still needed to be elaborated.
METHODS: The expression of HOTAIR and miR-143-3p were detected in cervical cancer tissues and cells by qRT-PCR. MTT and flow cytometry analysis were performed to measure cell proliferation and apoptosis. Bioinformatics, Dual-Luciferase reporter and RIP were used to analyze the possible correlation between HOTAIR, miR-143-3p and BCL2. The expression of Bax and BCL2 was detected by western blot. Mice xenograft model was established to confirm the role of HOTAIR on tumor growth in vivo.
RESULTS: HOTAIR expression was elevated while miR-143-3p expression was reduced in cervical cancer tissues and cell lines. HOTAIR knockdown suppressed proliferation and enhanced apoptosis in cervical cancer cells. Moreover, HOTAIR could function as a sponge for miR-143-3p. The inhibitory effect of HOTAIR knockdown on cervical cancer cells growth was abolished following decrease of miR-143-3p expression. Furthermore, HOTAIR promoted BCL2 expression by modulating miR-143-3p. BCL2 overexpression attenuated the tumor-suppressive effect of miR-143-3p in cervical cancer. Finally, the carcinogenicity of HOTAIR was validated in mice.
CONCLUSIONS: HOTAIR promoted cervical cancer cell growth by modulating BCL2 via miR-143-3p, hinting a novel regulatory mechanism and potential therapeutic target in cervical cancer.

PMID: 29336659 [PubMed - as supplied by publisher]

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