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2017 ; 17
(ä): 44
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Long non-coding RNA MALAT1 drives gastric cancer progression by regulating HMGB2
modulating the miR-1297
#MMPMID28396617
Li J
; Gao J
; Tian W
; Li Y
; Zhang J
Cancer Cell Int
2017[]; 17
(ä): 44
PMID28396617
show ga
BACKGROUND: Emerging evidences have verified that long non-coding RNAs (lncRNAs)
play important regulatory roles in the pathogenesis and progression of cancers.
lncRNAs metastasis associated lung adenocarcinoma transcript 1 (MALAT1) have been
found to be up-regulated in some human cancers. The main objective of this study
was to investigate the expression level and biological function of MALAT1 in
gastric cancer (GC). METHODS: Quantificational real-time polymerase chain
reaction (qRT-PCR) was performed to detect the mRNA levels of MALAT1 in 78 paired
gastric carcinoma tissues and adjacent normal tissues, and the associations of
MALAT1 expression with the clinicopathological features were analyzed, and the
prognosis of gastric carcinoma patients was evaluated. The HMGB2 mRNA and protein
expressions were detected by qRT-PCR and western-blot analysis. Luciferase
reporter assay was used to determine miR-1297 was a target of MALAT1. RESULTS: In
this study, we demonstrated MALAT1 was up-regulation in GC tissues compared with
adjacent normal tissues and higher MALAT1 expression was correlated with local
invasion, lymph node metastasis and TNM stage. Patients with higher MALAT1
expression predicted a shorter survival and poor prognosis. Functionally, we
revealed that MALAT1 promoted cells proliferation and invasion in GC.
Mechanistically, our results demonstrated that MALAT1 was negatively correlation
with miR-1297 and functioned as a molecular sponging miR-1297, antagonizing its
ability to suppress HMGB2 expression. CONCLUSIONS: Taken together, these results
demonstrated that MALAT1/miR-1297/HMGB2 axis acted as critical regulator pathway
in GC tumorigenesis and progression, which provided a novel therapeutic target
for gastric cancer.
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