De-Zheng Liu, Lin Wang, Shu-Kuan Yang, Zi-Jian Zhao, Yang-Yang Cui, Xue-Kai Zhao, Fan Zhang, Qing-Hai Guan, Lei Zhou
{"title":"MiR-451a靶向mex-3 RNA结合家族成员C，调控人肝母细胞瘤G2细胞的生长和转移。","authors":"De-Zheng Liu, Lin Wang, Shu-Kuan Yang, Zi-Jian Zhao, Yang-Yang Cui, Xue-Kai Zhao, Fan Zhang, Qing-Hai Guan, Lei Zhou","doi":"10.5306/wjco.v16.i9.111742","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Aim: </strong>To study the effect of miR-451a in liver cancer development.</p><p><strong>Methods: </strong>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 <i>via</i> wound scratch assay. Target gene was explored by bioinformatic analysis, and downstream molecule of miR-451a in liver cancer identified by rescue experiments.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>Therefore, miR-451a may be candidate miRNA for understanding molecular mechanisms of liver cancer development and novel target in liver cancer cell.</p>","PeriodicalId":23802,"journal":{"name":"World journal of clinical oncology","volume":"16 9","pages":"111742"},"PeriodicalIF":3.2000,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12476587/pdf/","citationCount":"0","resultStr":"{\"title\":\"MiR-451a targets mex-3 RNA binding family member C to regulate human hepatoblastoma G2 cell growth and metastasis.\",\"authors\":\"De-Zheng Liu, Lin Wang, Shu-Kuan Yang, Zi-Jian Zhao, Yang-Yang Cui, Xue-Kai Zhao, Fan Zhang, Qing-Hai Guan, Lei Zhou\",\"doi\":\"10.5306/wjco.v16.i9.111742\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>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.</p><p><strong>Aim: </strong>To study the effect of miR-451a in liver cancer development.</p><p><strong>Methods: </strong>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 <i>via</i> wound scratch assay. Target gene was explored by bioinformatic analysis, and downstream molecule of miR-451a in liver cancer identified by rescue experiments.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>Therefore, miR-451a may be candidate miRNA for understanding molecular mechanisms of liver cancer development and novel target in liver cancer cell.</p>\",\"PeriodicalId\":23802,\"journal\":{\"name\":\"World journal of clinical oncology\",\"volume\":\"16 9\",\"pages\":\"111742\"},\"PeriodicalIF\":3.2000,\"publicationDate\":\"2025-09-24\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12476587/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"World journal of clinical oncology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.5306/wjco.v16.i9.111742\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"World journal of clinical oncology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5306/wjco.v16.i9.111742","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"ONCOLOGY","Score":null,"Total":0}
MiR-451a targets mex-3 RNA binding family member C to regulate human hepatoblastoma G2 cell growth and metastasis.
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.
期刊介绍：
The WJCO is a high-quality, peer reviewed, open-access journal. The primary task of WJCO is to rapidly publish high-quality original articles, reviews, editorials, and case reports in the field of oncology. In order to promote productive academic communication, the peer review process for the WJCO is transparent; to this end, all published manuscripts are accompanied by the anonymized reviewers’ comments as well as the authors’ responses. The primary aims of the WJCO are to improve diagnostic, therapeutic and preventive modalities and the skills of clinicians and to guide clinical practice in oncology. Scope: Art of Oncology, Biology of Neoplasia, Breast Cancer, Cancer Prevention and Control, Cancer-Related Complications, Diagnosis in Oncology, Gastrointestinal Cancer, Genetic Testing For Cancer, Gynecologic Cancer, Head and Neck Cancer, Hematologic Malignancy, Lung Cancer, Melanoma, Molecular Oncology, Neurooncology, Palliative and Supportive Care, Pediatric Oncology, Surgical Oncology, Translational Oncology, and Urologic Oncology.
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