MicroRNA-642a-5p Targets DNA Damage-Inducible Transcript 4 to Suppress Hepatitis B Virus Hepatoma Carcinoma Cell

被引:0
|
作者
Ding, Min [1 ]
Yang, Juan [2 ]
Zeng, XueLi [3 ]
Liu, Pei [3 ]
Zhang, ShunLing [3 ]
Zheng, Sheng [2 ]
机构
[1] WuHan Univ, Wuhan Hosp 3, Tongren Hosp, Dept Oncol, Wuhan 430060, Hubei, Peoples R China
[2] Third Peoples Hosp Yunnan Prov, Dept Gastroenterol, 292 Beijing Rd, Kunming 650011, Yunnan, Peoples R China
[3] Dali Univ, Grad Sch Clin Med, Dali 671000, Yunnan, Peoples R China
关键词
Hepatitis B Virus; Liver Cancer; MicroRNA-642a-5p; DNA Damage -Inducible Transcript 4; HEPATOCELLULAR-CARCINOMA; EXPRESSION; PROLIFERATION; METHYLATION; APOPTOSIS; INVASION;
D O I
10.5812/jjm-145798
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Background: Hepatocellular carcinoma (HCC) is one of the most prevalent malignant tumors in clinical practice, with hepatitis B virus (HBV) being the most common risk factor for HCC. MicroRNAs (miRNAs) have emerged as a new marker for disease diagnosis and molecularly targeted therapies; however, the mechanism of miR 642a-5p in HBV-associated HCC remains unclear. Objectives: The aim of this study was to investigate the expression of miR 642a-5p, which targets DNA damage-inducible transcript 4 (DDIT4), in HBV-associated HCC, and its effect on the proliferation, migration, and invasion of HBV-positive HCC cells. Methods: miR 642a-5p in the serum of patients with HBV-associated liver cancer (LC), as well as miR 642a-5p and DDIT4 mRNA in LC tissues and cells, and HBV DNA in HBV-positive cells were detected. The targeting of DDIT4 by miR 642a-5p and the progression of cells were also examined. All cell experiments were repeated five times. Results: The results indicated that levels of miR 642a-5p were decreased, while levels of DDIT4 were increased in the serum, tissues, and cells of HBV-positive HCC patients. Overexpression of miR 642a-5p inhibited the progression of HBV-positive HCC cells, suppressed HBV DNA replication, cell proliferation, and invasion, and promoted apoptosis in HepG2.2.15 cells. Conclusions: In addition, miR 642a-5p directly targeted DDIT4, and knockdown of DDIT4 reversed the effects of miR 642a-5p upregulation, promoting the progression of HBV-positive HCC cells. In conclusion, miR 642a-5p is expressed at low levels in HBV-associated HCC and inhibits HBV DNA replication and tumor progression in HBV-positive HCC by targeting DDIT4. This study provides a foundation for molecular targeted therapy in HBV-positive HCC.
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页数:12
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