miR-21 targets Fas ligand-mediated apoptosis in breast cancer cell line MCF-7.
10.1007/s11596-014-1257-5
- Author:
Ming-fu WU
1
;
Jie YANG
;
Tao XIANG
;
Yan-yan SHI
;
Li-jiang LIU
Author Information
1. Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China, wumingfuwh@aliyun.com.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
genetics;
Breast Neoplasms;
genetics;
Fas Ligand Protein;
biosynthesis;
metabolism;
Female;
Flow Cytometry;
Gene Expression Regulation, Neoplastic;
Humans;
MCF-7 Cells;
MicroRNAs;
biosynthesis;
genetics;
Signal Transduction
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2014;34(2):190-194
- CountryChina
- Language:English
-
Abstract:
Over-expression of Fas ligand (FasL) on tumor cell surface can induce the apoptosis of specific activated tumor infiltrating lymphocytes (TILs) via the Fas/FasL pathway, leading to the formation of a site of immune privilege surrounding the tumor mass for escaping immune surveillance and promoting tumor proliferation, invasion and metastasis. The blocking effect of miR-21 on FasL-mediated apoptosis in breast cancers was investigated in this study. The expression levels of miR-21 and FasL in human breast carcinoma cell lines were detected by using RT-PCR and Western blotting. FasL as a target gene of miR-21 was identified by Luciferase assay. The apoptosis of Jurkat T lymphocytes induced by MCF-7 cells was determined by flow cytometry. It was found that in four human breast cancer cell lines, FasL expression level in MCF-7 cells was the highest, while miR-21 was down-regulated the most notably. After miR-21 expression in MCF-7 cells was up-regulated, FasL was identified as a target gene of miR-21. When the effector/target (E/T) ratio of MCF-7 cells and Jurkat cells was 10:1, 5:1 and 1:1, the inhibitory rate of apoptosis of Jurkat T lymphocytes induced by MCF-7 cells was 95.81%, 93.16% and 91.94%, respectively. It is suggested that in breast cancers miR-21 expression is negatively associated with FasL expression, and FasL is a target gene of miR-21. miR-21 targeting and regulating FasL-mediated apoptosis will bring us the possibility of a new tumor immunotherapy via breaking tumor immune privilege.
