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2018 ; 40
(1
): 61-72
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MicroRNA-125b inhibits cell proliferation and induces cell apoptosis in
esophageal squamous cell carcinoma by targeting BMF
#MMPMID29749531
Fan YX
; Bian XH
; Qian PD
; Chen ZZ
; Wen J
; Luo YH
; Yan PW
; Zhang Q
Oncol Rep
2018[Jul]; 40
(1
): 61-72
PMID29749531
show ga
MicroRNAs (miRNAs) have been reported to regulate the expression of genes by
suppressing translation or facilitating mRNA decay. Their expression regulates a
wide variety of cellular processes, including the development and progression of
cancer. Esophageal squamous cell carcinoma (ESCC) is a malignant cancer with high
morbidity and recurrence in Asia. In the present study, the biological function
of miR-125b and its underlying mechanism in ESCC were explored. The results
revealed that miR-125b expression was significantly decreased in ESCC tissues and
cell lines. A decrease in miR-125b was markedly related to lymphatic metastasis
in patients. Functional analysis revealed that the overexpression of miR-125b
using miR-125b mimics significantly inhibited cell growth and induced cell
apoptosis, and increased the G1 phase of the cell cycle in EC109 and EC9706
cells. Notably, the miR-125b inhibitors revealed the opposite effect.
Additionally, overexpression of miR-125b significantly inhibited tumor growth
in vivo. Furthermore, BCL-2-modifying factor (BMF) was considered to be a
potential candidate target of miR-125b based on miRNA target databases. miR-125b
negatively regulated BMF expression by directly binding to its 3'-untranslated
region. BMF was a functional target of miR-125b in the regulation of cell
proliferation, cell apoptosis and the cell cycle in EC109 and EC9706 cells. In
clinical ESCC specimens, BMF expression was upregulated, and negatively
correlated with that of miR-125b. In conclusion, miR-125b had an antitumor role
in ESCC cells mediated by targeting BMF, which can be potentially useful for
tumorigenesis in ESCC.
|Adaptor Proteins, Signal Transducing/*genetics
[MESH]