An Inventive Report of Inducing Apoptosis in Non-Small Cell Lung Cancer (NSCLC) Cell Lines by Transfection of MiR-4301

肺癌 细胞凋亡 转染 流式细胞术 细胞培养 癌症研究 细胞生长 MTT法 细胞 A549电池 小RNA 癌症 生物 分子生物学 活力测定 化学 病理 医学 生物化学 基因 遗传学
作者
Abbas Jamshidi Avval,Ahmad Majd,Naghmeh Gholipour,Kambiz Akbari Noghabi,Anna Ohradanova‐Repic,Ghasem Ahangari
出处
期刊:Anti-cancer Agents in Medicinal Chemistry [Bentham Science]
卷期号:19 (13): 1609-1617 被引量:3
标识
DOI:10.2174/1871520619666190416114145
摘要

Background: Based on recent studies, new therapeutic strategies have been developed for cancer treatment using microRNAs (miRNAs). With this view, miRNAs manipulating techniques can be considered as novel therapeutic prospects for cancer treatment. In this study, we evaluated the expression of miR-4301 in human lung cancer cell lines and investigated its potential role in cell proliferation and tumor suppression on Non-Small Cell Lung Cancer (NSCLC) cells. Methods: We used quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) to examine the level of miR- 4301 expression in human lung cancer cell lines (A549, QU-DB) and non-malignant lung epithelial cells (HFLF-PI5). Then, we investigated the effect of miR-4301 by transfecting it into these cell lines and probing for cancer cell viability and apoptosis using the MTT assay, flow cytometry and immunofluorescence staining. Results: Our results showed that the expression level of miR-4301 was significantly reduced in human lung cancer cell lines (P<0.001). When miR-4301 was transfected in lung cancer cells, their cell proliferation was suppressed and apoptosis induced. This decline in cell survival was confirmed by the MTT assay. Transfection of miR-4301 caused an increase in early and late apoptotic cells in all lung cancer cell lines tested. Conclusion: Our findings show that miR-4301 may act as a lung cancer suppressor through targeting of proteins involved in cell proliferation and survival. For this reason, targeting miR-4301 may provide a new strategy for the diagnosis and treatment of patients with this deadly disease. This article is protected by copyright. All rights reserved.
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