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Title: Long non-coding RNA linc00673 regulated non-small cell lung cancer proliferation, migration, invasion and epithelial mesenchymal transition by sponging miR-150-5p
Authors: Lu, W
Zhang, H
Niu, Y
Wu, Y
Sun, W
Li, H
Kong, J
Ding, K
Shen, H.-M 
Wu, H
Xia, D
Wu, Y
Keywords: long untranslated RNA
microRNA 150
transforming growth factor beta
unclassified drug
long untranslated RNA
MIRN150 microRNA, human
transcription factor ZEB1
ZEB1 protein, human
animal cell
animal experiment
animal model
animal tissue
cancer prognosis
cancer survival
cell invasion assay
cell migration
cell proliferation
cell proliferation assay
controlled study
epithelial mesenchymal transition
gene expression
gene overexpression
human cell
human tissue
in vitro study
in vivo study
luciferase assay
non small cell lung cancer
quantitative analysis
reverse transcription polymerase chain reaction
tumor invasion
Western blotting
wound healing assay
biological model
cell motion
cell proliferation
cell survival
epithelial mesenchymal transition
gene expression regulation
lung tumor
non small cell lung cancer
nucleotide sequence
survival analysis
tumor cell line
tumor invasion
Base Sequence
Carcinoma, Non-Small-Cell Lung
Cell Line, Tumor
Cell Movement
Cell Proliferation
Cell Survival
Epithelial-Mesenchymal Transition
Gene Expression Regulation, Neoplastic
Lung Neoplasms
Models, Biological
Neoplasm Invasiveness
RNA, Long Noncoding
Survival Analysis
Zinc Finger E-box-Binding Homeobox 1
Issue Date: 2017
Citation: Lu, W, Zhang, H, Niu, Y, Wu, Y, Sun, W, Li, H, Kong, J, Ding, K, Shen, H.-M, Wu, H, Xia, D, Wu, Y (2017). Long non-coding RNA linc00673 regulated non-small cell lung cancer proliferation, migration, invasion and epithelial mesenchymal transition by sponging miR-150-5p. Molecular Cancer 16 (1) : 118. ScholarBank@NUS Repository.
Rights: Attribution 4.0 International
Abstract: Background: The function of a new long non-coding RNA linc00673 remains unclear. While identified as an oncogenic player in non-small cell lung cancer (NSCLC), linc00673 was found to be anti-oncogenic in pancreatic ductal adenocarcinoma (PDAC). However whether linc00673 regulated malignancy and epithelial mesenchymal transition (EMT) has not been characterized. Methods: Cell proliferation was assessed using CCK-8 and EdU assays, and cell migration and invasion were assessed using scratch assays and transwell invasion assays. Epithelial mesenchymal transition was examined using western blot, qRT-PCR and immunofluorescence staining. Interaction between miRNA and linc00673 was determined using luciferase reporter assays. In vivo experiments were performed to assess tumor formation. In addition, the expression data of NSCLC specimens of TCGA and patient survival data were utilized to explore the prognostic significance of linc00673. Results: In the present study, we found high linc00673 expression was associated with poor prognosis of NSCLC patients. In vitro experiments showed linc00673 knockdown reversed TGF-β induced EMT, and miR-150-5p was predicted to target linc00673 through bioinformatics tools. Overexpression of miR-150-5p suppressed lin00673's expression while inhibition of miR-150-5p led to significant upregulation of lin00673, suggesting that linc00673 could be negatively regulated by miR-150-5p, which was further confirmed by the inverse correlation between linc00673 and miR-150-5p in NSCLC patients' specimen. Furthermore, we proved that miR-150-5p could directly target linc00673 through luciferase assay, so linc00673 could sponge miR-150-5p and modulate the expression of a key EMT regulator ZEB1 indirectly. In addition, miR-150-5p inhibition abrogated linc00673 silence mediated proliferation, migration, invasion and EMT suppressing effect. Moreover, the inhibition of linc00673 significantly attenuated the tumorigenesis ability of A549 cells in vivo. Conclusions: We validated linc00673 as a novel oncogenic lncRNA and demonstrated the molecular mechanism by which it promotes NSCLC, which will advance our understanding of its clinical significance. © 2017 The Author(s).
Source Title: Molecular Cancer
ISSN: 14764598
DOI: 10.1186/s12943-017-0685-9
Rights: Attribution 4.0 International
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