HPV16 E6 regulates miR-23a expression and promotes invasion and migration of cervical cancer cells
10.3969/j.issn.1006-5725.2024.02.004
- VernacularTitle:HPV16 E6调控miR-23a表达促进宫颈癌细胞侵袭、迁移
- Author:
Min WANG
1
;
Dan MU
;
Dejun KONG
;
Li YANG
;
Lu YE
;
Dan HE
Author Information
1. 成都医学院第二附属医院/核工业四一六医院肿瘤科 (成都 610000)
- Keywords:
human papillomavirus 16 E6 protein;
miR-23a;
cervical cancer;
invasion;
migration
- From:
The Journal of Practical Medicine
2024;40(2):146-152
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of high-risk human papillomavirus 16 E6 protein(HPV16 E6 protein)on invasion and migration of cervical cancer SiHa cells via regulating the expression of expression miR-23a.Methods Tissue samples from 100 patients with cervical cancer HPV-negative,100 HPV-positive patients,and 100 paracancerous normal tissues were collected;cervical cancer SiHa cells were divided into blank group,E6 overexpression group,negative transfection group,and E6 + miR-23a mimics group.The expression of miR-23a and HPV16 E6 mRNA were detected by qRT-PCR;MTT assay was used to detect the cell proliferation inhibition rate;flow cytometry to detect the apoptosis;Transwell chamber assay to detect cell invasion,and scratch test to detect the ability of cell migration.The expression of HPV16 E6,apoptosis related proteins(Caspase-3,Bax,Bcl-2),and migration related proteins(MMP-2,MMP-9)was detected by WB.Results The expression level of miR-23a was decreased in cervical cancer tissues,and that was lower in HPV positive cervical cancer tissues.Overexpression of E6 decreased the expression level of miR-23a,cell proliferation inhibition rate,apoptosis rate,Caspase-3 and Bax protein expression,and increased the expression of Bcl-2 protein,scratch healing rate,inva-sion cell number,MMP-2,MMP-9 protein expression(P<0.05);miR-23a mimics reversed the effects of E6 overexpression on the above indicators.Conclusion HPV16 E6 promotes the invasion and migration of cervical cancer cells,which may be related to the regulation of miR-23a expression.
