LINC00852 通过与 miR-140-3p 竞争结合来调节 AGTR1 表达，促进卵巢癌细胞的增殖和侵袭。
LINC00852 promotes the proliferation and invasion of ovarian cancer cells by competitively binding with miR-140-3p to regulate AGTR1 expression.
机构信息
Department of Gynaecology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Insititute, No.44, Xiaoheyan Road, Shenyang, 110042, Liaoning Province, China.
出版信息
BMC Cancer. 2021 Sep 8;21(1):1004. doi: 10.1186/s12885-021-08730-7.
BACKGROUND
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.
METHODS
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.
RESULTS
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.
CONCLUSION
LINC00852/miR-140-3p/AGTR1 is an important pathway to promote the proliferation and invasion of ovarian cancer.
背景
长链非编码 RNA（lncRNAs）的失调已在卵巢癌中被发现。然而，LINC00852 在卵巢癌中的表达和生物学功能尚不清楚。
方法
通过实时定量逆转录聚合酶链反应（qRT-PCR）检测卵巢癌组织和细胞中 LINC00852、miR-140-3p 和 AGTR1mRNA 的表达。体外进行增益和缺失功能测定，以探讨 LINC00852 和 miR-140-3p 在卵巢癌进展中的生物学功能。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 LINC00852 和 miR-140-3p 之间的结合。
结果
我们发现 LINC00852 在卵巢癌组织和细胞中的表达显著上调，而 miR-140-3p 在卵巢癌组织中的表达显著下调。功能上，LINC00852 敲低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，并负调控卵巢癌细胞中的其水平。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 敲低抑制卵巢癌在体内的生长和侵袭。
结论
LINC00852/miR-140-3p/AGTR1 是促进卵巢癌增殖和侵袭的重要途径。
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