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微小RNA-148a-3p靶向CEMIP以抑制胃癌细胞的发生。

MiR-148a-3p targets CEMIP to suppress the genesis of gastric cancer cells.

作者信息

Song Ming, Liu Jun, Zheng Xin, Zhou Xin, Feng Zehui, Hu Wei

机构信息

Department of General Surgery, Wuhan Third Hospital, Wuhan, 430000, Hubei, China.

Department of General Surgery, Dongfeng Hospital of Hubei University of Medicine, Wuhan, 430000, Hubei, China.

出版信息

Biochem Biophys Res Commun. 2021 Oct 20;575:42-49. doi: 10.1016/j.bbrc.2021.08.039. Epub 2021 Aug 18.

DOI:10.1016/j.bbrc.2021.08.039
PMID:34455220
Abstract

BACKGROUND

Gastric cancer is the sixth common malignancy worldwide. Dysregulation of Cell Migration Inducing Hyaluronidase 1 (CEMIP) gene and microRNA-148a -3p (miR-148a-3p) expressions has been found in gastric cancer genesis. However, the underlying molecular mechanism in gastric cancer needs further investigation.

METHODS

The expression of gastric cancer tissues' and cells' CEMIP and miR-148a-3p were examined by RT-qPCR. The interaction between miR-148a-3p and CEMIP was verified by luciferase activity detection. Cell viability, proliferation, adhesion, and apoptosis in gastric cancer GTL-16 and AGS cells were analyzed by CCK8, BrdU, cell adhesion, and FITC assay.

RESULTS

CEMIP expression was significantly elevated, but the miR-148a-3p level was downregulated in gastric cancer tissues and cell lines. Overexpression of CEMIP accelerated cell viability, proliferation, and adhesion, but attenuated cell apoptosis of gastric cancer cells. In addition, upregulation of miR-148a-3p repressed the development of gastric cancer in vitro. Moreover, miR-148a-3p suppressed gastric cancer tumorigenesis by inhibiting the expression of CEMIP.

CONCLUSION

The study clarified that miR-148a-3p suppressed gastric cancer tumorigenesis by inhibiting CEMIP, which may be effective targets for the clinical treatment of gastric cancer.

摘要

背景

胃癌是全球第六大常见恶性肿瘤。已发现在胃癌发生过程中细胞迁移诱导透明质酸酶1(CEMIP)基因和微小RNA - 148a - 3p(miR - 148a - 3p)表达失调。然而,胃癌潜在的分子机制仍需进一步研究。

方法

通过逆转录定量聚合酶链反应(RT - qPCR)检测胃癌组织和细胞中CEMIP和miR - 148a - 3p的表达。通过荧光素酶活性检测验证miR - 148a - 3p与CEMIP之间的相互作用。采用细胞计数试剂盒8(CCK8)、5 - 溴脱氧尿嘧啶核苷(BrdU)、细胞黏附及异硫氰酸荧光素(FITC)检测法分析胃癌GTL - 16和AGS细胞的活力、增殖、黏附及凋亡情况。

结果

CEMIP在胃癌组织和细胞系中的表达显著升高,但miR - 148a - 3p水平下调。CEMIP的过表达加速了胃癌细胞的活力、增殖和黏附,但减弱了其凋亡。此外,miR - 148a - 3p的上调在体外抑制了胃癌的发展。而且,miR - 148a - 3p通过抑制CEMIP的表达抑制胃癌肿瘤发生。

结论

该研究阐明miR - 148a - 3p通过抑制CEMIP抑制胃癌肿瘤发生,这可能是胃癌临床治疗的有效靶点。

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