Dysregulation of long non-coding RNAs (lncRNAs) has been identified in ovarian cancer. However, the expression and biological functions of LINC00852 in ovarian cancer are not understood. The expressions of LINC00852, miR-140-3p and AGTR1 mRNA in ovarian cancer tissues and cells were detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR) assay. Gain- and loss-of-function assays were performed to explore the biological functions of LINC00852 and miR-140-3p in the progression of ovarian cancer in vitro. The bindings between LINC00852 and miR-140-3p were confirmed by luciferase reporter gene assay, RNA immunoprecipitation (RIP) assay and RNA pull-down assay. We found that LINC00852 expression was significantly up-regulated in ovarian cancer tissues and cells, whereas miR-140-3p expression was significantly down-regulated in ovarian cancer tissues. Functionally, LINC00852 knockdown inhibited the viability, proliferation and invasion of ovarian cancer cells, and promoted the apoptosis of ovarian cancer cells. Further investigation showed that LINC00852 interacted with miR-140-3p, and miR-140-3p overexpression suppressed the viability, proliferation and invasion of ovarian cancer cells. In addition, miR-140-3p interacted with AGTR1 and negatively regulated its level in ovarian cancer cells. Mechanistically, we found that LINC00852 acted as a ceRNA of miR-140-3p to promote AGTR1 expression and activate MEK/ERK/STAT3 pathway. Finally, LINC00852 knockdown inhibited the growth and invasion ovarian cancer in vivo. LINC00852/miR-140-3p/AGTR1 is an important pathway to promote the proliferation and invasion of ovarian cancer.

中文翻译：

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LINC00852通过与miR-140-3p竞争性结合调节AGTR1表达促进卵巢癌细胞增殖和侵袭

已在卵巢癌中发现长链非编码 RNA (lncRNA) 的失调。然而，LINC00852在卵巢癌中的表达和生物学功能尚不清楚。采用定量逆转录聚合酶链反应（qRT-PCR）法检测卵巢癌组织和细胞中LINC00852、miR-140-3p和AGTR1 mRNA的表达。进行了功能获得和功能丧失检测，以探索 LINC00852 和 miR-140-3p 在体外卵巢癌进展中的生物学功能。LINC00852 和 miR-140-3p 之间的结合通过荧光素酶报告基因测定、RNA 免疫沉淀 (RIP) 测定和 RNA 下拉测定证实。我们发现LINC00852在卵巢癌组织和细胞中的表达显着上调，而miR-140-3p的表达在卵巢癌组织中显着下调。在功能上，敲低LINC00852可抑制卵巢癌细胞的活力、增殖和侵袭，促进卵巢癌细胞的凋亡。进一步研究表明，LINC00852与miR-140-3p相互作用，miR-140-3p过表达抑制卵巢癌细胞的活力、增殖和侵袭。此外，miR-140-3p 与 AGTR1 相互作用并负调节其在卵巢癌细胞中的水平。在机制上，我们发现 LINC00852 作为 miR-140-3p 的 ceRNA 促进 AGTR1 表达并激活 MEK/ERK/STAT3 通路。最后，LINC00852敲低抑制了体内卵巢癌的生长和侵袭。