IRF1受到miR-23a调控抑制舌鳞癌细胞增殖并促进凋亡

doi:10.3969/j.issn.1006-6233.2022.04.010

Abstract
Figure/Table
References
Related Citation (15)

Download: PDF (1915 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

Abstract Objective: To study the effect of IRF1 gene on proliferation and apoptosis of tongue squamous carcinoma cells and its upstream regulation mechanism by miR-23a. Methods: The expression level of IRF1 gene was detected by Real-time PCR in tongue squamous carcinoma tissues. The overexpression plasmid of IRF1 was constructed, and the effects of IRF1 on proliferation and apoptosis of tongue squamous carcinoma cells were examined by MTT assay and TUNEL assay, respectively. Bioinformatic predictions as well as fluorescent reporter vector assays verified that IRF1 was a direct target gene for miR-23a. The expression level of miR-23a in tongue squamous carcinoma tissues and the alteration of proliferation and apoptosis of tongue squamous carcinoma cells after the expression of miR-23a was further examined.Results: IRF1 expression levels were significantly lower in tongue squamous carcinoma tissues compared to paraneoplastic normal tissues. Overexpression of IRF1 in tongue squamous carcinoma cells resulted in a significant decrease in cell growth activity and an increase in paclitaxel-induced apoptosis index. TargetScan predicted that miR-23a could bind to the 3 'UTR of IRF1. It was confirmed that miR-23a could directly bind to the 3'UTR of IRF1 and thus regulate the expression of IRF1. The expression of miR-23a was abnormally elevated in tongue squamous carcinoma tissues, and after the expression of miR-23a was blocked, the growth activity of tongue squamous carcinoma cells was significantly decreased, while the apoptosis index induced by paclitaxel was increased, which was consistent with the results obtained from overexpression of IRF1. Conclusion: IRF1 is regulated by miR-23a to inhibit the growth activity and promote apoptosis of tongue squamous carcinoma cells. IRF1 is a tumor suppressor gene in the occurrence and development of tongue squamous cell carcinoma, while miR-23a, as an upstream regulator of IRF1, is also an oncogene of tongue squamous cell carcinoma.

Key words： IRF1 TSCC Proliferation Apoptosis

	Service

	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors

Cite this article:

URL:

http://www.hbyxzzs.cn/EN/10.3969/j.issn.1006-6233.2022.04.010 OR http://www.hbyxzzs.cn/EN/Y2022/V28/I4/578

[1] Almangush A,Heikkinen I,Makitie AA,et al.Prognostic biomarkers for oral tongue squamous cell carcinoma:a systematic review and meta-analysis[J].Br Cancer,2017,117(6):856~866.
[2] Almahmoudi R,Salem A,Murshid S,et al.Interleukin-17F has anti-tumor effects in oral tongue cancer[J].Cancers (Basel),2019,11(5):650.
[3] 郭俊峰,张纲,谭颖徽.CYP27B1在口腔鳞状细胞癌中的表达及其与预后的关系[J].口腔医学研究,2020,36(10):930~933.
[4] 常晴晴.早期舌鳞癌颈淋巴结隐匿性转移的临床病理分析[D].河北医科大学,2019.
[5] 王文天,赵慧娟,杨洋,池颖,张磊.过表达干扰素调节因子IRF1重塑K562细胞的稳态特征[J].中国实验血液学杂志,2020,28(1):51~55.
[6] Huang JX,Wu YC,Cheng YY,et al.IRF1 negatively regulates oncogenic KPNA2 expression under growth stimulation and hypoxia in lung cancer cells[J].Onco Targets Ther,2019,12:11475~11486.
[7] Zhou Y,Wang Q,Chu L,et al. FOXM1c promotes oesophageal cancer metastasis by transcriptionally regulating IRF1 expression[J].Cell Prolif,2019,52(2):e12553.
[8] Cui M,Yao X,Lin Y,et al.Interactive functions of microRNAs in the miR-23a-27a-24-2 cluster and the potential for targeted therapy in cancer[J].Cell Physiol,2020,235(1):6~16.
[9] He Q,Chen Z,Dong Q,et al.MicroRNA-21 regulates prostaglandin E2 signaling pathway by targeting 15-hydroxyprostaglandin dehydrogenase in tongue squamous cellcarcinoma[J].BMC Cancer,2016,16(1):685.
[10] Korvala J,Jee K,Porkola E,et al.MicroRNA and protein profiles in invasive versus non-invasive oral tongue squamous cell carcinoma cells in vitro[J].Exp Cell Res,2017,350(1):9~18.
[11] Hu X,Wang Y,Liang H,et al.miR-23a/b promote tumor growth and suppress apoptosis by targeting PDCD4 in gastric cancer[J].Cell Death Dis,2017,8(10):e3059.
[12] Wei Y,Chen X,Yang J,et al.DcR3 promotes proliferation and invasion of pancreatic cancer via a DcR3/STAT1/IRF1 feedback loop[J].Am Cancer Res,2019,9(12):2618~2633.
[13] Szekely B,Bossuyt V,Li X,et al.Immunological differences between primary and metastatic breast cancer[J].Ann Oncol,2018,29(11):2232~2239.