Dong Xiaogang, Ding Wei, Ye Jianwei, Yan Dong, Xue Feng, Xu Lin, Yin Jiwei, Guo Wenjia
Department of Hepatopancreatobiliary Surgery, Cancer Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China.
Department of Cancer Center, The first affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China.
Cell Biochem Funct. 2016 Oct;34(7):491-496. doi: 10.1002/cbf.3213. Epub 2016 Sep 21.
Dysregulation of microRNAs has been demonstrated to contribute to malignant progression of cancers, including hepatocellular carcinoma (HCC). MiR-24-3p was previously reported to be significantly upregulated in HCC. However, the potential role and mechanism of action of miR-24-3p in the initiation and progression of HCC remain largely unknown. Quantitative reverse transcription polymerase chain reaction demonstrated that miR-24-3p was significantly upregulated in HCC tumor tissues compared with nontumor tissues. The cell viability, colony formation assay, and tumorigenicity assays in nude mice showed that miR-24-3p could enhance HCC cell growth in vitro and in vivo. Metallothionein 1M was verified as an miR-24-3p target gene by using dual-luciferase reporter assays, quantitative reverse transcription polymerase chain reaction, and Western blotting, which was involved in miR-24-3p regulated HCC cell growth. These results indicated that miR-24-3p plays an important role in the initiation and progression of HCC by targeting metallothionein 1M, and the miR-24-3p/metallothionein 1M pathway may contribute to the development of novel therapeutic strategies for HCC in the future.
微小RNA的失调已被证明与包括肝细胞癌(HCC)在内的癌症恶性进展有关。先前有报道称miR-24-3p在HCC中显著上调。然而,miR-24-3p在HCC发生和发展中的潜在作用及作用机制仍 largely未知。定量逆转录聚合酶链反应表明,与非肿瘤组织相比,miR-24-3p在HCC肿瘤组织中显著上调。细胞活力、集落形成试验和裸鼠致瘤性试验表明,miR-24-3p可在体外和体内增强HCC细胞生长。通过双荧光素酶报告基因试验、定量逆转录聚合酶链反应和蛋白质免疫印迹法验证金属硫蛋白1M是miR-24-3p的靶基因,其参与了miR-24-3p调控的HCC细胞生长。这些结果表明,miR-24-3p通过靶向金属硫蛋白1M在HCC的发生和发展中起重要作用,并且miR-24-3p/金属硫蛋白1M途径可能有助于未来开发针对HCC的新型治疗策略。