LINC00665通过调控miRNA-34a-5p/E2F3轴促进卵巢癌进展。
LINC00665 promotes Ovarian Cancer progression through regulating the miRNA-34a-5p/E2F3 axis.
作者信息
Xu Dan, Song Qingxia, Liu Ying, Chen Wansu, Lu Lijuan, Xu Min, Fang Xiaohui, Zhao Wenjie, Zhou Huifang
机构信息
Department of Gynaecology, Suzhou TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Suzhou 215009, China.
Nanjing University of Chinese Medicine, Nanjing, 210023, China.
出版信息
J Cancer. 2021 Jan 18;12(6):1755-1763. doi: 10.7150/jca.51457. eCollection 2021.
To clarify the role of LINC00665 in ovarian cancer (OC) progression and the possible mechanism. LINC00665 levels in OC tissues and cell lines were detected by qRT-PCR. The correlation between LINC00665 and clinicopathologic characteristics of OC patients was assessed. Biological functions of OC cell phenotypes influenced by LINC00665 were examined by CCK-8, colony formation and Transwell assay. Dual-luciferase reporter assay and RIP assay were conducted to verify the interaction between LINC00665 and its downstream target. LINC00665 was upregulated in OC and linked to poor prognosis. Knockdown of LINC00665 blocked malignant proliferative, migratory and invasive functions of OC cells. By competitively binding miRNA-34a-5p, LINC00665 abolished the inhibitory effect of miR-34a-3p on its downstream gene E2F3, thus promoting OC progression. LINC00665/miRNA-34a-5p/E2F3 axis is involved in OC progression, providing novel insights into the clinical treatment of OC.
为阐明LINC00665在卵巢癌（OC）进展中的作用及可能机制。采用qRT-PCR检测OC组织和细胞系中LINC00665的水平。评估LINC00665与OC患者临床病理特征之间的相关性。通过CCK-8、集落形成和Transwell实验检测受LINC00665影响的OC细胞表型的生物学功能。进行双荧光素酶报告基因实验和RIP实验以验证LINC00665与其下游靶点之间的相互作用。LINC00665在OC中上调并与不良预后相关。敲低LINC00665可阻断OC细胞的恶性增殖、迁移和侵袭功能。通过竞争性结合miRNA-34a-5p，LINC00665消除了miR-34a-3p对其下游基因E2F3的抑制作用，从而促进OC进展。LINC00665/miRNA-34a-5p/E2F3轴参与OC进展，为OC的临床治疗提供了新的见解。
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