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miR-494-3p诱导人口腔鳞状癌细胞发生细胞衰老并增强其放射敏感性。

miR-494-3p Induces Cellular Senescence and Enhances Radiosensitivity in Human Oral Squamous Carcinoma Cells.

作者信息

Weng Jui-Hung, Yu Cheng-Chia, Lee Yueh-Chun, Lin Cheng-Wei, Chang Wen-Wei, Kuo Yu-Liang

机构信息

Department of Nuclear Medicine, Chung Shan Medical University Hospital, Taichung 40201, Taiwan.

School of Dentistry, Chung Shan Medical University, Taichung 40201, Taiwan.

出版信息

Int J Mol Sci. 2016 Jul 8;17(7):1092. doi: 10.3390/ijms17071092.

DOI:10.3390/ijms17071092
PMID:27399693
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4964468/
Abstract

Oral squamous cell carcinoma (OSCC) is the most common malignancy of head and neck. Although radiotherapy is used for OSCC treatment, the occurrence of radioresistant cancer cells limits its efficiency. MicroRNAs (miRNAs) are non-coding RNAs with lengths of 18-25 base pairs and known to be involved in carcinogenesis. We previously demonstrated that by targeting B lymphoma Mo-MLV insertion region 1 homolog (Bmi1), miR-494-3p functions as a putative tumor suppressor miRNA in OSCC. In this study, we further discovered that miR-494-3p could enhance the radiosensitivity of SAS OSCC cells and induce cellular senescence. The overexpression of miR-494-3p in SAS cells increased the population of senescence-associated β-galactosidase positive cells, the expression of p16(INK4a) and retinoblastoma 1 (RB1), as well as downregulated Bmi1. The knockdown of Bmi1 by lentiviral-mediated delivery of specific short hairpin RNAs (shRNAs) also enhanced the radiosensitivity of SAS cells and the activation of the senescence pathway. Furthermore, the inverse correlation between Bmi1 and miR-494-3p expression was observed among OSCC tissues. Results suggest that miR-494-3p could increase the radiosensitivity of OSCC cells through the induction of cellular senescence caused by the downregulation of Bmi1.

摘要

口腔鳞状细胞癌（OSCC）是头颈部最常见的恶性肿瘤。尽管放射疗法用于OSCC的治疗，但放射抗性癌细胞的出现限制了其疗效。微小RNA（miRNA）是长度为18 - 25个碱基对的非编码RNA，已知参与致癌过程。我们之前证明，通过靶向B淋巴瘤Mo - MLV插入区域1同源物（Bmi1），miR - 494 - 3p在OSCC中作为一种假定的肿瘤抑制性miRNA发挥作用。在本研究中，我们进一步发现miR - 494 - 3p可增强SAS OSCC细胞的放射敏感性并诱导细胞衰老。miR - 494 - 3p在SAS细胞中的过表达增加了衰老相关β - 半乳糖苷酶阳性细胞的数量、p16（INK4a）和视网膜母细胞瘤1（RB1）的表达，并下调了Bmi1。通过慢病毒介导的特异性短发夹RNA（shRNA）传递敲低Bmi1也增强了SAS细胞的放射敏感性和衰老途径的激活。此外，在OSCC组织中观察到Bmi1与miR - 494 - 3p表达之间呈负相关。结果表明，miR - 494 - 3p可通过下调Bmi1诱导细胞衰老来增加OSCC细胞的放射敏感性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd01/4964468/e4aeba00ff9c/ijms-17-01092-g006.jpg
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