LncRNA LINC00665 Promotes Ovarian Cancer Cell Proliferation and Inhibits Apoptosis via Targeting miR-181a-5p/FHDC

被引:11
作者
Wang, Suli [1 ,2 ]
Wang, Yingchun [3 ]
Lu, Jin [2 ]
Wang, Jinhua [2 ]
机构
[1] Nanjing Med Univ, Nanjing Matern & Child Hlth Care Hosp, Dept Womens Hlth, Womens Hosp, Nanjing 210004, Jiangsu, Peoples R China
[2] Nanjing Med Univ, Affiliated Canc Hosp, Jiangsu Inst Canc Res, Dept Gynecol Oncol Surg,Jiangsu Canc Hosp, 42 Baiziting Rd, Nanjing 210009, Jiangsu, Peoples R China
[3] Nanjing Matern & Child Hlth Care Hosp, Dept Gynecol, Nanjing 210004, Jiangsu, Peoples R China
关键词
LINC00665; miR-181a-5p; FHDC1; Human ovarian cancer; LONG NONCODING RNA; PROGRESSION; EXPRESSION; MIGRATION; INVASION; MIRNA; GENE;
D O I
10.1007/s12010-022-03943-3
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Previous reports indicate that long intergenic non-coding RNA LINC00665 naturally occurred vital effects in various cancers. Herein, the role of LINC00665 in ovarian cancer progress was explored. We found that LINC00665 was upregulated in ovarian cancer cell lines. Besides, a series of assays including flow cytometry, wound-healing, transwell, cell counting Kit-8 (CCK-8), and EdU assay confirmed that the knockdown of LINC00665 could reduce the viability, proliferation, and migration of SKOV-3 and OVCAR-3 cells. Accumulating evidence indicates that many lncRNAs can function as endogenous miRNA sponges by competitively binding common miRNAs. In this study, the bioinformatics analysis suggests that LNC00665 specifically binds to miR-181a-5p. LINC00665 downregulated the miR-181a-5p in SKOV-3 and OVCAR-3 cells. The knockdown of miR-181a-5p evidently reverses the inhibitory effect of sh-LINC00662. Besides, FH2 domain containing 1 (FHDC1) has been proved to deed as an effective target of miR-181a-5p. The results reveal the knockdown of LINC00665 facilitates ovarian cancer via development by sponging miR-181a-5p and up-regulating FHDC1 expression. These may contribute to ovarian cancer therapy.
引用
收藏
页码:3819 / 3832
页数:14
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