MicroRNA‑490‑3p suppresses the proliferation and invasion of hepatocellular carcinoma cells via targeting TMOD3
- Honghua Wang
- Guobao Yang
- Yang Yu
- Peibing Gu
Affiliations: Department of General Surgery, Xiangshui County People's Hospital, Yancheng, Jiangsu 224600, P.R. China
- Published online on: August 6, 2020 https://doi.org/10.3892/ol.2020.11956
Copyright: © Wang
et al. This is an open access article distributed under the
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Commons Attribution License.
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Hepatocellular carcinoma (HCC) is a primary malignancy of the liver. It has been reported that microRNAs (miRs) play important roles in the progression and development of HCC. The expression of miR‑490‑3p has been shown to be downregulated in HCC tissues. Therefore, the present study aimed to investigate the effects of miR‑490‑3p on HCC cells and the underlying mechanism. Cell Counting Kit‑8, flow cytometry, and Transwell migration and invasion assays were performed to determine the viability, apoptosis, migration and invasion of HCC cells, respectively. Furthermore, a luciferase activity assay was used to verify the association between miR‑490‑3p and its predicted target tropomodulin 3 (TMOD3). In addition, the protein levels of Bax, Bcl‑2, cleaved caspase‑3, TMOD3, phosphorylated (p)‑p38 and p‑ERK in HCC cells were detected using western blot analysis. The results demonstrated that the overexpression of miR‑490‑3p via transfection with miR‑490‑3p mimics significantly inhibited the proliferation of Huh‑7 and HEP 3B2.1‑7 cells. In addition, overexpression of miR‑490‑3p markedly suppressed the migration and invasion abilities of Huh‑7 cells. miR‑490‑3p mimics significantly induced liver cancer cell apoptosis via upregulating Bax and cleaved caspase‑3 and downregulating anti‑apoptotic protein Bcl‑2. Additionally, a luciferase activity assay indicated that TMOD3 is a downstream target gene of miR‑490‑3p. The protein levels of TMOD3, p‑p38 and p‑ERK were significantly downregulated in Huh‑7 cells following transfection with miR‑490‑3p mimics, and the overexpression of TMOD3 attenuated these effects. In conclusion, the aforementioned results suggest that the overexpression of miR‑490‑3p inhibited the proliferation and invasion of HCC cells by targeting TMOD3. Therefore, the miR‑490‑3p/TMOD3 axis may be a potent target for the treatment of HCC.