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长链非编码 RNA CASC15 通过靶向 miR-101-3p 促进宫颈癌细胞的增殖并诱导其凋亡。

Long non-coding RNA CASC15 promotes proliferation and induces apoptosis of cervical cancer cells through targeting miR-101-3p.

机构信息

Department of Obstetrics and Gynecology, Hubei Public Security County People's Hospital, Gongan County, China.

出版信息

Eur Rev Med Pharmacol Sci. 2020 Jan;24(2):611-618. doi: 10.26355/eurrev_202001_20037.

DOI:10.26355/eurrev_202001_20037
PMID:32016962
Abstract

OBJECTIVE

Cervical cancer (CC) is a common type of fatal gynecological cancer worldwide. The aim of this study was to identify the exact role of lncRNA CASC15 in the progression of CC and to explore the possible underlying mechanism.

PATIENTS AND METHODS

Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was used to detect CASC15 expression in 4 CC cell lines, and 54 paired CC tissue samples. The roles of CASC15 in CC were explored through apoptosis assay, colony formation assay, and proliferation assay in vitro, respectively. Furthermore, the underlying mechanism of CASC15 in CC was explored by luciferase reporter gene assay and RNA immunoprecipitation (RIP) assay.

RESULTS

CASC15 expression in CC tissues was remarkably higher than that of adjacent normal tissues. The knockdown of CASC15 significantly inhibited CC cell proliferation, whereas induced cell apoptosis in vitro. Meanwhile, CC cell proliferation was remarkably promoted, and cell apoptosis was inhibited by overexpression of CASC15 in vitro. In addition, miR-101-3p was up-regulated and down-regulated after knockdown and overexpression of CASC15 in vitro, respectively. Furthermore, bioinformatics analysis and mechanism assays revealed that miR-101-3p was a direct target of CASC15 in CC tumorigenesis.

CONCLUSIONS

CASC15 could promote proliferation and inhibit apoptosis of CC cells by targeting miR-101-3p. Our findings suggested that CASC15 might offer a new therapeutic intervention for CC patients.

摘要

目的

宫颈癌(CC)是一种常见的致命妇科癌症,在全球范围内。本研究旨在确定 lncRNA CASC15 在 CC 进展中的的确切作用,并探讨其可能的潜在机制。

患者和方法

实时定量聚合酶链反应(RT-qPCR)用于检测 4 种 CC 细胞系和 54 对 CC 组织样本中的 CASC15 表达。通过体外凋亡试验、集落形成试验和增殖试验分别探讨 CASC15 在 CC 中的作用。此外,通过荧光素酶报告基因检测和 RNA 免疫沉淀(RIP)试验探讨 CASC15 在 CC 中的潜在机制。

结果

CC 组织中的 CASC15 表达明显高于相邻正常组织。CASC15 敲低显著抑制 CC 细胞增殖,而体外诱导细胞凋亡。同时,过表达 CASC15 可显著促进 CC 细胞增殖,抑制细胞凋亡。此外,体外敲低和过表达 CASC15 后,miR-101-3p 表达水平分别上调和下调。此外,生物信息学分析和机制试验表明,miR-101-3p 是 CC 肿瘤发生中 CASC15 的直接靶标。

结论

CASC15 可能通过靶向 miR-101-3p 促进 CC 细胞的增殖和抑制凋亡。我们的研究结果表明,CASC15 可能为 CC 患者提供新的治疗干预措施。

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Eur Rev Med Pharmacol Sci. 2020 Jan;24(2):611-618. doi: 10.26355/eurrev_202001_20037.
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