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MiR-202 functions as a tumor suppressor in hepatocellular carcinoma by targeting HK2.

ABSTRACT: Recent evidence has suggested that microRNAs (miRNAs) can participate in metabolic reprogramming. Additionally, aerobic glycolysis is associated with tumor progression in hepatocellular carcinoma (HCC). In the present study, miRNA (miR)-202 expression levels were found to be significantly lower in HCC tissues compared with the corresponding adjacent non-cancerous tissue samples using reverse transcription-quantitative PCR analysis in 56 patients with HCC. Lower miR-202 expression levels were identified to be associated with tumor size, vascular invasion, Tumor, Node and Metastasis stages and poor overall survival rates in patients with HCC. In vitro, upregulation of miR-202 expression was revealed to significantly suppress the cell glucose uptake, lactate production and cell proliferation in liver cancer cells. In addition, dual luciferase reporter analysis and western blot assays suggested that hexokinase 2 (HK2) was a direct target of miR-202. Upregulation of miR-202 expression could inhibit cell proliferation by regulating HK2 expression in HCC. Therefore, the results from the present study suggested that miR-202 may serve as a potential target for HCC treatment.

SUBMITTER: Wang J

PROVIDER: S-EPMC7039053 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature

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miR-202 functions as a tumor suppressor in hepatocellular carcinoma by targeting HK2.

Wang Jiangang J Chen Jili J Sun Fang F Wang Zhiwei Z Xu Wenfang W Yu Yafeng Y Ding Feng F Shen Huajiang H

Oncology letters 20200123 3

Recent evidence has suggested that microRNAs (miRNAs) can participate in metabolic reprogramming. Additionally, aerobic glycolysis is associated with tumor progression in hepatocellular carcinoma (HCC). In the present study, miRNA (miR)-202 expression levels were found to be significantly lower in HCC tissues compared with the corresponding adjacent non-cancerous tissue samples using reverse transcription-quantitative PCR analysis in 56 patients with HCC. Lower miR-202 expression levels were ide ...[more]

PMID: 32194725

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Project description:BACKGROUND:Liver cancer is among the most common malignancy worldwide. Hepatocellular carcinoma (HCC), the principal histological subtype of liver cancer, is globally the third most common cause of cancer-related mortality. The high rates of recurrence and metastasis contribute to the poor prognosis of HCC patients. In recent years, increasing evidence has shown that microRNAs (miRNAs) are involved in the tumorigenesis, progression, and prognosis of HCC. METHODS:To screen for key candidate miRNAs in HCC, three microarray datasets were downloaded from Gene Expression Omnibus (GEO). The sole common differentially expressed miRNA (DEmiR) observed in the above three datasets using a Venn diagram was microRNA-211-5p (miR-211-5p). The expression of miR-211-5p from HCC tissues was measured in several HCC cell lines. Additionally, using Kaplan-Meier plots, the potential prognostic value of miR-211-5p in HCC was analyzed. Cell counting kit-8 (CCK-8) and transwell assays examined the ability of miR-211-5p to induce cell proliferation, migration, and invasion in HCC cultures. The interaction of miR-211-5p and Acyl-CoA Synthetase Long Chain Family Member 4 (ACSL4) was assessed both theoretically and using a luciferase reporter assay. Finally, the ability of miR-211-5p to modulate tumorigenesis in HCC in vivo was assessed after establishing a xenograft model. RESULTS:qRT-PCR demonstrated that the relative expression of miR-211-5p was considerably down-regulated in HCC tissues and cell lines compared with normal tissue. Kaplan-Meier plots indicated that HCC patients with decreased expression of miR-211-5p had poor overall survival. Upregulation of miR-211-5p in vitro consistently suppressed cell proliferation, migration, and invasion. In contrast, enhanced expression of ACSL4 promoted a malignant phenotype in HCC cells. Importantly, we discovered that ACSL4 was a direct downstream target of miR-211-5p in HCC, and that miR-211-5p suppressed the malignant phenotype by inhibition of ACSL4 expression. Furthermore, miR-211-5p overexpression impaired tumorigenesis and growth of HCC in vivo. CONCLUSIONS:Targeting miR-211-5p and the downstream gene ACSL4 will possibly provide novel insight and represents a promising approach to future therapy of HCC patients.

Dataset Information

MiR-202 functions as a tumor suppressor in hepatocellular carcinoma by targeting HK2.

Publications

miR-202 functions as a tumor suppressor in hepatocellular carcinoma by targeting HK2.

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