
Function of microRNA‑141 in human breast cancer through cytotoxic CD4+ T cells regulated by MAP4K4 expression
Author(s) -
Qing Zhang,
Xiaohong Huang,
Fuchou Tang
Publication year - 2018
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2018.8814
Subject(s) - oncogene , downregulation and upregulation , cancer research , microrna , biology , cytotoxic t cell , cancer , cancer cell , protein kinase a , breast cancer , tumor necrosis factor alpha , cell cycle , kinase , immunology , microbiology and biotechnology , biochemistry , genetics , in vitro , gene
The present study investigated the anti‑cancer effect of microRNA (miRNA)‑141 on apoptosis rate of breast cancer cells and the possible underlying mechanism. In patients with breast cancer, the expression of miRNA‑141 was downregulated. Overexpression of miRNA‑141 reduced breast cancer cell growth, inhibited the expression of cyclooxygenase‑2 (COX‑2), prostaglandin E2 (PGE2) and tumor necrosis factor (TNF)‑α, and increased the expression levels of interleukin (IL)‑10. However, downregulation of miRNA‑141 resulted in upregulation of COX‑2, PGE2 and TNF‑α expression levels, and an inhibition of IL‑10. Overexpression of miRNA‑141 suppressed mitogen‑activated protein kinase kinase kinase kinase 4 (MAP4K4) protein expression. Downregulation of miRNA‑141 markedly upregulated MAP4K4 protein expression in MCF‑7 cells. Promotion of MAP4K4 protein expression reduced the effects of miRNA‑141 on the toxicity of CD4+ T cells on breast cancer cells. The results of the present study indicated that miRNA‑141 may cause anti‑tumor effects in human breast cancer cells via cytotoxic CD4+ T cells.