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下调长链非编码 RNA CCAT5 通过抑制 STAT3 抑制结直肠癌细胞的生长、侵袭和转移。

Downregulating long non-coding RNA CCAT5 inhibits tumor growth, invasion and metastasis in colorectal cancer through suppressing STAT3.

机构信息

Department of Outpatient, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.

出版信息

Eur Rev Med Pharmacol Sci. 2019 Sep;23(18):7899-7904. doi: 10.26355/eurrev_201909_19001.

Abstract

OBJECTIVE

Recent researches have proved that long noncoding RNAs (lncRNAs) play an important role in tumorigenesis. In this research, lncRNA CCAT5 was explored to identify its role in the development of colorectal cancer (CRC).

PATIENTS AND METHODS

Real time-quantitative polymerase chain reaction (RT-qPCR) was utilized to measure CCAT5 expression of CRC tissues. Besides, function assays including wound healing assay and transwell assay were conducted. Furthermore, RT-qPCR and Western blot assay were used to explore the underlying mechanism.

RESULTS

By comparison with CCAT5 expression in adjacent tissues, the CCAT5 expression level was significantly higher in CRC samples. Moreover, after CCAT5 was downregulated, cell migration and cell invasion of CRC cells were suppressed. Besides, after knockdown of CCAT5, the mRNA and protein expression of STAT3 was repressed. Furthermore, it was found that STAT3 expression was positively correlated to CCAT5 expression in CRC tissues.

CONCLUSIONS

Results suggest that CCAT5 could promote cell migration and invasion of CRC by upregulating STAT3, which may offer a potential therapeutic target in CRC.

摘要

目的

最近的研究证明长链非编码 RNA(lncRNA)在肿瘤发生中起重要作用。本研究探索 lncRNA CCAT5 以确定其在结直肠癌(CRC)发展中的作用。

患者与方法

采用实时定量聚合酶链反应(RT-qPCR)测量 CRC 组织中 CCAT5 的表达。此外,还进行了包括划痕愈合试验和 Transwell 试验在内的功能测定。进一步采用 RT-qPCR 和 Western blot 检测来探索潜在的机制。

结果

与相邻组织中的 CCAT5 表达相比,CRC 样本中的 CCAT5 表达水平显著更高。此外,下调 CCAT5 后,CRC 细胞的迁移和侵袭能力受到抑制。此外,下调 CCAT5 后,STAT3 的 mRNA 和蛋白表达受到抑制。此外,还发现 CRC 组织中 STAT3 表达与 CCAT5 表达呈正相关。

结论

结果表明,CCAT5 通过上调 STAT3 促进 CRC 细胞的迁移和侵袭,这可能为 CRC 提供一个潜在的治疗靶点。

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