NDLI: MicroRNA-125b may function as an oncogene in lung cancer cells.

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MicroRNA-125b may function as an oncogene in lung cancer cells.

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MicroRNA-125b may function as an oncogene in lung cancer cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Zhang, Juan Yin, Lihong Pu, Yuepu Liang, Geyu Zhang, Yanqiu Wang, Xikai Fu, Yanyun
Description	Author Affiliation: Wang X ( Key Laboratory of Environmental Medicine Engineering Ministry of Education, School of Public Health, Southeast University, Nanjing, Jiangsu 210009, P.R. China.); Zhang Y ( Key Laboratory of Environmental Medicine Engineering Ministry of Education, School of Public Health, Southeast University, Nanjing, Jiangsu 210009, P.R. China.); Fu Y ( Key Laboratory of Environmental Medicine Engineering Ministry of Education, School of Public Health, Southeast University, Nanjing, Jiangsu 210009, P.R. China.); Zhang J ( Key Laboratory of Environmental Medicine Engineering Ministry of Education, School of Public Health, Southeast University, Nanjing, Jiangsu 210009, P.R. China.); Yin L ( Key Laboratory of Environmental Medicine Engineering Ministry of Education, School of Public Health, Southeast University, Nanjing, Jiangsu 210009, P.R. China.); Pu Y ( Key Laboratory of Environmental Medicine Engineering Ministry of Education, School of Public Health, Southeast University, Nanjing, Jiangsu 210009, P.R. China.); Liang G ( Key Laboratory of Environmental Medicine Engineering Ministry of Education, School of Public Health, Southeast University, Nanjing, Jiangsu 210009, P.R. China.)
Abstract	The present study aimed to investigate the biofunctions of microRNA (miR)125b on lung cancer cells. A miR genechip array was used to examine the differential expression of miRs between 95D lung cancer cells and 16 human bronchial epithelial (HBE) cells. Overexpression of miR125b was observed in the cell lines and in the lung carcinoma tissues compared with the adjacent tissues, confirmed using reverse transcription quantitative polymerase chain reaction. Bioinformatic analysis of miR125b was also performed, including target prediction, gene ontology and pathway analysis. MTT, flow cytometry and Transwell assays were also used to examine the effect of downregulated miR125b on the proliferation, apoptosis, invasive ability and cell cycle of 95D cells. Significant differences were observed in the expression of 45 miRs in the 95D cells compared with those in 16HBE cells and the expression of miR125b was significantly higher in 95D cells compared with that in 16HBE cells as well as in lung tumor tissues compared with that in adjacent tissues. In addition, inhibition of the expression of miR125b in 95D cells induced apoptosis, G1/S phase arrest and reduction of their invasive ability. In addition, bioinformatics software predicted that miR125b was involved in the regulation of several pathways associated with cancer, including the transforming growth factorß, Wnt and mitogenactivated protein kinase signaling pathways. These data indicated for the first time, to the best of our knowledge, that miR125b may function as an oncogene in lung cancer.
ISSN	17912997
e-ISSN	17913004
Journal	Molecular Medicine Reports
Issue Number	5
Volume Number	11
Language	English
Publisher	Spandidos Publications
Publisher Date	2015-05-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Lung Neoplasms Genetics Micrornas Oncogenes Apoptosis Cell Cycle Cell Line, Tumor Cell Proliferation Computational Biology Gene Expression Gene Expression Profiling Metabolism Transforming Growth Factor Beta Wnt Signaling Pathway Research Support, Non-u.s. Gov't Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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