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2018 ; 22
(3
): 1527-1537
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LncRNA-DANCR contributes to lung adenocarcinoma progression by sponging miR-496
to modulate mTOR expression
#MMPMID29266795
Lu QC
; Rui ZH
; Guo ZL
; Xie W
; Shan S
; Ren T
J Cell Mol Med
2018[Mar]; 22
(3
): 1527-1537
PMID29266795
show ga
Long non-coding RNAs (lncRNAs) have emerged as new and important regulators of
pathological processes including tumour development. In this study, we
demonstrated that differentiation antagonizing non-protein coding RNA (DANCR) was
up-regulated in lung adenocarcinoma (ADC) and that the knockdown of DANCR
inhibited tumour cell proliferation, migration and invasion and restored cell
apoptosis rescued; cotransfection with a miR-496 inhibitor reversed these
effects. Luciferase reporter assays showed that miR-496 directly modulated DANCR;
additionally, we used RNA-binding protein immunoprecipitation (RIP) and RNA
pull-down assays to further confirm that the suppression of DANCR by miR-496 was
RISC-dependent. Our study also indicated that mTOR was a target of miR-496 and
that DANCR could modulate the expression levels of mTOR by working as a competing
endogenous RNA (ceRNA). Furthermore, the knockdown of DANCR reduced tumour
volumes in vivo compared with those of the control group. In conclusion, this
study showed that DANCR might be an oncogenic lncRNA that regulates mTOR
expression through directly binding to miR-496. DANCR may be regarded as a
biomarker or therapeutic target for ADC.
|*Gene Expression Regulation, Neoplastic
[MESH]
|Adenocarcinoma of Lung/*genetics/metabolism/pathology
[MESH]