MiR-451a targets mex-3 RNA binding family member C to regulate human hepatoblastoma G2 cell growth and metastasis

doi:10.5306/wjco.v16.i9.111742

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World Journal of Clinical Oncology

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World J Clin Oncol. Sep 24, 2025; 16(9): 111742
Published online Sep 24, 2025. doi: 10.5306/wjco.v16.i9.111742

MiR-451a targets mex-3 RNA binding family member C to regulate human hepatoblastoma G2 cell growth and metastasis

De-Zheng Liu, Lin Wang, Shu-Kuan Yang, Zi-Jian Zhao, Yang-Yang Cui, Xue-Kai Zhao, Fan Zhang, Qing-Hai Guan, Lei Zhou

De-Zheng Liu, Shu-Kuan Yang, Zi-Jian Zhao, Yang-Yang Cui, Fan Zhang, Qing-Hai Guan, Lei Zhou, Department of Biliary-Pancreatic Surgery, Binzhou Medical University Hospital, Binzhou 256603, Shandong Province, China

Lin Wang, Department of Ophthalmology, Binzhou Medical University Hospital, Binzhou 256603, Shandong Province, China

Xue-Kai Zhao, Department of Hepatobiliary Surgery, Binzhou People's Hospital, Binzhou 256603, Shandong Province, China

Author contributions: Liu DZ, Wang L, Yang SK, Zhao ZJ and Zhou L designed the study and drafted the manuscript; Liu DZ, Wang L, Yang SK, Zhao ZJ, Cui YY, Zhao XK, Zhang F, Guan QH and Zhou L performed the research; all authors read and approved the final manuscript.

Supported by National Natural Science Foundation of China, No. 31640052; and Natural Science Foundation of Shandong Province, China, No. ZR2019BH031.

Institutional review board statement: The study was reviewed and approved by Research Ethics Committee of Binzhou Medical University Hospital, No. 2024-S36-001.

Conflict-of-interest statement: The author reports no conflicts of interest in this work.

Data sharing statement: The data that support the findings of this study are available on request from the corresponding author, upon reasonable request.

Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/

Corresponding author: Lei Zhou, MD, PhD, Full Professor, Department of Biliary-Pancreatic Surgery, Binzhou Medical University Hospital, No. 661 Huanghe 2^nd Road, Binzhou 256603, Shandong Province, China. dr_zhlei@163.com

Received: July 9, 2025
Revised: July 26, 2025
Accepted: August 22, 2025
Published online: September 24, 2025
Processing time: 77 Days and 5.7 Hours

Abstract

BACKGROUND

Aberrant microRNAs expression and associated pathways have been proved participate in regulation vast various physiologic and pathologic processed of different human cancers including liver cancer. While, the function of miR-451a in liver cancer still indistinct.

AIM

To study the effect of miR-451a in liver cancer development.

METHODS

GeneChip microarray analysis performed to detect miR-451a expression in liver cancer tissues and normal liver tissues. Reverse transcription-polymerase chain reaction was used to validate the expression of miR-451a in liver cancer cell and other tumor cell lines. Construction of liver cancer cell lines that stably overexpressed miR-451a by transfecting Lentivirus produced by Genechem company. Methylthiazolyldiphenyl-tetrazolium (MTT) bromide assay and colony formation assay to determine the effect of miR-451a in liver cancer cell proliferation. Flow cytometry used to investigate whether miR-451a involved in liver cancer cell apoptosis. Cell migration ability was measured via wound scratch assay. Target gene was explored by bioinformatic analysis, and downstream molecule of miR-451a in liver cancer identified by rescue experiments.

RESULTS

MiR-451a expression significantly downregulation in liver cancer tissues compared with that in normal liver tissue. MiR-451a also obviously low-expressed in liver cancer cell, colorectal carcinoma cell and esophageal carcinoma cell lines. Human hepatoblastoma G2 (HepG2) and BEL-7404 cell lines that stably overexpressed miR-451a by transfecting lentivirus constructed successfully. MTT bromide assay and colony formation assay showed that the overexpressed miR-451a inhibit HepG2 cell proliferation viability, but not BEL-7404 cell. Flow cytometry determined that miR-451a regulating proliferation not through inducing apoptosis. Wound scratch assay revealed that miR-451a overexpression suppressed HepG2 cell migration. Furthermore, mex-3 RNA binding family member C was predicted as the target gene by bioinformatic analysis, and rescue experiments confirmed the hypothesis.

CONCLUSION

Therefore, miR-451a may be candidate miRNA for understanding molecular mechanisms of liver cancer development and novel target in liver cancer cell.

Keywords: Liver cancer; MiR-451a; Mex-3 RNA binding family member C; Proliferation; Migration

Core Tip: Aberrant microRNAs expression and associated pathways have been proved participate in regulation vast various physiologic and pathologic processed of different human cancers including liver cancer. In this study, we first provided evidence that miR-451a obviously down-regulated in hepatocellular carcinoma (HCC) tissues and tumor cell lines. Overexpression of miR-451a significantly inhibit human hepatoblastoma G2 (HepG2) cell proliferation, colony formation and migration. However, miR-451a were not participated in HCC cell apoptosis. Moreover, bioinformatic analysis showed that mex-3 RNA binding family member C (MEX3C) was target gene of miR-451a, which validated by reverse transcription-polymerase chain reaction and western blotting. Furthermore, rescue experiments confirmed that overexpression of MEX3C can inhibit the effect of miR-451a in HepG2.