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Knockdown of long non-coding RNA HOTAIR increases miR-454-3p by targeting Stat3
and Atg12 to inhibit chondrosarcoma growth
#MMPMID28182000
Bao X
; Ren T
; Huang Y
; Sun K
; Wang S
; Liu K
; Zheng B
; Guo W
Cell Death Dis
2017[Feb]; 8
(2
): e2605
PMID28182000
show ga
Current practices for the therapy of chondrosarcoma, including wide-margin
surgical resection and chemotherapy, are less than satisfactory. Recently,
emerging evidence has demonstrated that long non-coding RNAs (lncRNAs) have an
essential role in the initiation and progression of tumors. As a typical lncRNA,
HOTAIR is significantly overexpressed in various tumors. However, the function
and potential biological mechanisms of HOTAIR in human chondrosarcoma remain
unknown. Quantitative RT-PCR demonstrated that HOTAIR expression was upregulated
in chondrosarcoma tissues and cell lines. High HOTAIR expression is correlated
with tumor stage and poor prognosis. Functional experiments reveal that HOTAIR
knockdown leads to growth inhibition of human chondrosarcoma cells in vitro and
in vivo. In addition to cycle arrest and apoptosis, knockdown of HOTAIR inhibits
autophagy, which favors cell death. Mechanistically, we demonstrated that HOTAIR
induced DNA methylation of miR-454-3p by recruiting EZH2 and DNMT1 to the
miR-454-3p promoter regions, which markedly silences miR-454-3p expression.
Further analysis revealed that STAT3 and ATG12 are targets of miR-454-3p,
initiate HOTAIR deficiency-induced apoptosis and reduce autophagy. Collectively,
our data reveal the roles and functional mechanisms of HOTAIR in human
chondrosarcoma and suggest that HOTAIR may act as a prognostic biomarker and
potential therapeutic target for chondrosarcoma.
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