World journal of clinical oncology · 2025
MiR-451a targets mex-3 RNA binding family member C to regulate human hepatoblastoma G2 cell growth and metastasis.
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Liu De-Zheng, Wang Lin, Yang Shu-Kuan, Zhao Zi-Jian, Cui Yang-Yang, Zhao Xue-Kai, Zhang Fan, Guan Qing-Hai, Zhou Lei
Аннотация
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.
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.