» Articles » PMID: 31372052

MicroRNA-218 Regulates the Chemo-sensitivity of Cervical Cancer Cells Through Targeting Survivin

Overview
Publisher Dove Medical Press
Specialty Oncology
Date 2019 Aug 3
PMID 31372052
Citations 12
Authors
Affiliations
Soon will be listed here.
Abstract

Cervical cancer is one of the most lethal malignancies among women in the world. Every year about 311,365 women die because of cervical cancer. Chemo-resistance is the main reason of the lethal malignancies, and the mechanism of chemo-resistance in cervical cancer still remains largely elusive. Previous studies reported that microRNAs played important biological roles in the chemo-resistance in many types of cancers, in the present study we tried to investigate the biological roles of microRNA-218 in chemo-resistance in cervical cancer cells. Real-time PCR results indicated microRNA-218 was downregulated in cisplatin-resistant HeLa/DDP and SiHa/DDP cells compared with the mock HeLa and SiHa cells. CCK-8 assay results showed upregulation of microRNA-218 enhanced the cisplatin sensitivity of cervical cancer cells; while downregulation of microRNA-218 decreased the cisplatin sensitivity of cervical cancer cells. Dual-luciferase assay indicated survivin was a direct target of microRNA-218. Western blotting and PCR results indicated the expression of survivin in HeLa/DDP and SiHa/DDP cells was significantly increased compared with HeLa and SiHa cells. Further study indicated induction of microRNA-218 decreased the expression of survivin while inhibition of microRNA-218 increased the expression of survivin in cervical cancer cells. Cell apoptosis results indicated induction of microRNA-218 induced the cell apoptosis in cervical cancer cells. Our data revealed microRNA-218 enhanced the cisplatin sensitivity in cervical cancer cells through regulation of cell growth and cell apoptosis, which could potentially benefit to the cervical cancer treatment in the future.

Citing Articles

Prognostic and clinicopathological significance of survivin in gynecological cancer.

Chuwa A, Mvunta D Oncol Rev. 2024; 18:1444008.

PMID: 39687493 PMC: 11646728. DOI: 10.3389/or.2024.1444008.


Relationship Between Expression of microRNA and Chemotherapy Resistance in Cervical Carcinoma.

Chao-Hui H, Jing L, Xue C, Ting-Shi W, Chong L Appl Biochem Biotechnol. 2022; 195(3):1928-1946.

PMID: 36401723 DOI: 10.1007/s12010-022-04227-6.


Diagnostic value of colposcopy in patients with cytology-negative and HR-HPV-positive cervical lesions.

Liu Y, Liao J, Yi X, Pan Z, Pan J, Sun C Arch Gynecol Obstet. 2022; 306(4):1161-1169.

PMID: 35320389 DOI: 10.1007/s00404-022-06415-5.


MicroRNA-92a-3p Enhances Cisplatin Resistance by Regulating Krüppel-Like Factor 4-Mediated Cell Apoptosis and Epithelial-to-Mesenchymal Transition in Cervical Cancer.

Yang J, Hai J, Dong X, Zhang M, Duan S Front Pharmacol. 2022; 12:783213.

PMID: 35095494 PMC: 8795743. DOI: 10.3389/fphar.2021.783213.


MiRNA-218 inhibits cell proliferation, migration and invasion by targeting Runt-related transcription factor 2 (Runx2) in human osteosarcoma cells.

Guo Q, Ma J, Wu J Regen Ther. 2022; 18:508-515.

PMID: 34977284 PMC: 8668442. DOI: 10.1016/j.reth.2021.11.003.


References
1.
Thomas G . Improved treatment for cervical cancer--concurrent chemotherapy and radiotherapy. N Engl J Med. 1999; 340(15):1198-200. DOI: 10.1056/NEJM199904153401509. View

2.
Martin-Martinez A, Molano F, LLoret M, Falcon-Vizcaino O, Garcia-Hernandez J . Concurrent chemotherapy and radiotherapy for cervical cancer. Eur J Gynaecol Oncol. 2003; 24(2):160-2. View

3.
Marusawa H, Matsuzawa S, Welsh K, Zou H, Armstrong R, Tamm I . HBXIP functions as a cofactor of survivin in apoptosis suppression. EMBO J. 2003; 22(11):2729-40. PMC: 156760. DOI: 10.1093/emboj/cdg263. View

4.
Lukka H, Johnston M . Concurrent cisplatin-based chemotherapy plus radiotherapy for cervical cancer: a meta-analysis. Clin Oncol (R Coll Radiol). 2004; 16(2):160-1. DOI: 10.1016/j.clon.2004.01.002. View

5.
Ellenson L, Wu T . Focus on endometrial and cervical cancer. Cancer Cell. 2004; 5(6):533-8. DOI: 10.1016/j.ccr.2004.05.029. View