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miR-122 通过抑制细胞周期蛋白 G1 来增敏肝癌细胞。

MiR-122 radiosensitize hepatocellular carcinoma cells by suppressing cyclin G1.

机构信息

Department of Radiation Oncology, Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, China.

出版信息

Int J Radiat Biol. 2022;98(1):11-17. doi: 10.1080/09553002.2021.1987561. Epub 2021 Oct 12.

DOI:10.1080/09553002.2021.1987561
PMID:34623217
Abstract

PURPOSE

Emerging evidence has shown that radiotherapy is an effective treatment for hepatocellular carcinoma (HCC), Micro(mi)RNAs are involved in regulating radiosensitivity in many cancers. MiR-122 accounts for approximately 70% of all cloned miRNAs in the liver, but there are few reports about whether it is involved in regulating of radiosensitivity in HCC cells.

MATERIALS AND METHODS

HCC cells (HepG2 and Huh7) overexpressing miR-122 were constructed by transfecting them with lentiviral-miR-122. Then, their proliferation ability was analyzed by the MTT, and colony formation assays and a xenograft tumor model was used to detect their radiosensitivity. The expression of cyclin G1 mRNA and protein was detected by the quantitative real-time polymerase chain reaction and western blotting, respectively.

RESULTS

Overexpression of miR-122 inhibited the proliferation of, and radiosensitized HCC cells. Cyclin G1 mRNA and protein level were suppressed in HepG2 tumors overexpression miR-122.

CONCLUSION

MiR-122 may be useful as a potential radiosensitizer for HCC, and its mechanism is related to the regulation of cyclin G1.

摘要

目的

新出现的证据表明,放射治疗是治疗肝细胞癌(HCC)的有效方法。Micro(mi)RNAs 参与调节许多癌症的放射敏感性。miR-122 约占肝脏中所有克隆 miRNAs 的 70%,但关于它是否参与调节 HCC 细胞的放射敏感性的报道很少。

材料和方法

通过慢病毒转染构建 miR-122 过表达的 HCC 细胞(HepG2 和 Huh7)。然后,通过 MTT、集落形成实验和异种移植肿瘤模型分析它们的增殖能力,检测它们的放射敏感性。通过实时定量聚合酶链反应和 Western blot 分别检测细胞周期蛋白 G1 mRNA 和蛋白的表达。

结果

miR-122 的过表达抑制了 HCC 细胞的增殖并放射增敏。miR-122 过表达的 HepG2 肿瘤中细胞周期蛋白 G1 mRNA 和蛋白水平受到抑制。

结论

miR-122 可能作为 HCC 的潜在放射增敏剂有用,其机制与 cyclin G1 的调节有关。

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