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2016 ; 15
(1
): 51
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MiR-143-3p functions as a tumor suppressor by regulating cell proliferation,
invasion and epithelial-mesenchymal transition by targeting QKI-5 in esophageal
squamous cell carcinoma
#MMPMID27358073
He Z
; Yi J
; Liu X
; Chen J
; Han S
; Jin L
; Chen L
; Song H
Mol Cancer
2016[Jun]; 15
(1
): 51
PMID27358073
show ga
BACKGROUND: Dysregulation of microRNAs (miRNAs) have been demonstrated to
contribute to carcinogenesis. MiR-143-3p has been identified to function as a
tumor suppressor in several tumors, but the role of miR-143-3p in esophageal
squamous cell carcinoma (ESCC) has not been intensively investigated. Our aim was
to evaluate the potential role of miR-143-3p in the progression of ESCC. METHODS:
The expression levels of miR-143-3p and QKI-5 protein were measured in 80
resected ESCC tumor specimens and the clinicopathological significance of these
levels determined. We also investigated the role of miR-143-3p in the regulation
of QKI-5 expression in ESCC cell lines both in vivo and in vitro. RESULTS:
MiR-143-3p levels were decreased in ESCC clinical samples and low expression of
miR-143-3p was significantly associated with poor prognosis in ESCC patients.
Ectopic expression of miR-143-3p suppressed proliferation and induced apoptosis
in ESCC cells both in vivo and in vitro. Ectopic expression of miR-143-3p also
reduced the metastatic potential of cells by selectively regulating
epithelial-mesenchymal transition regulatory proteins. Furthermore, QKI-5 isoform
was upregulated in ESCC tissues and was a direct target of miR-143-3p. Lastly,
re-introduction of QKI-5 expression abrogated the inhibitory effects of
miR-143-3p on ESCC cell proliferation and motility. CONCLUSIONS: Our results
demonstrate that miR-143-3p acts as a tumor-suppressor by targeting QKI-5 in
ESCC, suggesting that miR-143-3p is a potential therapy for the treatment of
ESCC.