LncRNA miR503HG Regulates the Drug Resistance of Recurrent Cervical Squamous Cell Carcinoma Cells by Regulating miR-155/Caspase-3

被引:7
作者
Zhao, Shanshan [1 ]
Yu, Mingxin [1 ]
Wang, Lei [1 ]
机构
[1] China Med Univ, Canc Hosp, Liaoning Canc Hosp & Inst, Gynaecol, 44 Xiaoheyan Rd, Shenyang 110042, Liaoning, Peoples R China
来源
CANCER MANAGEMENT AND RESEARCH | 2020年 / 12卷
关键词
cervical squamous cell carcinoma; miR503HG; miR-155; Caspase-3; apoptosis; CISPLATIN RESISTANCE; CANCER; APOPTOSIS; MIR-155; METASTASIS; EXPRESSION; CASPASE-3;
D O I
10.2147/CMAR.S225489
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Introduction: The purpose of this study is to investigate the role of long non-coding RNA (lncRNA) miR503 Host Gene (miR503HG) in cervical squamous cell carcinoma (CSCC). Methods: Analysis of TCGA dataset revealed that expression levels of miR503HG in CSCC tissues were over 12 times lower than those in non-tumor tissues, indicating its involvement in CSCC. Results: In this study, we observed that levels of miR503HG in plasma were significantly lower in CSCC patients than in healthy participants. The cisplatin-based treatment further down-regulated miR503HG in both patients and CSCC cells. MiR503HG overexpression in CSCC cells led to the suppression of miR-155 and elevation of Caspase-3, acting as the downstream target of miR-155. Cell apoptosis analysis showed that miR503HG and Caspase-3 overexpression led to an increased cell apoptosis rate under Cisplatin treatment. MiR-155 played the opposite role and attenuated the functions of Caspase-3 and miR503HG overexpression. Conclusion: Therefore, miR503HG may regulate the drug resistance of CSCC cells by regulating mir-155/Caspase-3.
引用
收藏
页码:1579 / 1585
页数:7
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