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LINC00968 can inhibit the progression of lung adenocarcinoma through the miR-21-5p/SMAD7 signal axis

Background: Long non-coding RNAs (LncRNAs) have been associated with several types of cancer. However, little is known about their role in lung adenocarcinoma (LUAD). Results: LINC00968 was significantly differentially expressed in LUAD tissues. Downregulated LINC00968 was associated with clinicopat...

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Autores principales: Zhu, Yuxing, Bo, Hao, Chen, Zhizhao, Li, Jingjing, He, Dong, Xiao, Mengqing, Xiang, Liang, Jin, Long, Zhou, Jianda, Gong, Lian, Zhou, Yanhong, Zhou, Ming, Xiong, Wei, Xing, Xiaowei, Li, Ruhong, Cao, Ke
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7695398/
https://www.ncbi.nlm.nih.gov/pubmed/33147570
http://dx.doi.org/10.18632/aging.104011
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author Zhu, Yuxing
Bo, Hao
Chen, Zhizhao
Li, Jingjing
He, Dong
Xiao, Mengqing
Xiang, Liang
Jin, Long
Zhou, Jianda
Gong, Lian
Zhou, Yanhong
Zhou, Ming
Xiong, Wei
Xing, Xiaowei
Li, Ruhong
Cao, Ke
author_facet Zhu, Yuxing
Bo, Hao
Chen, Zhizhao
Li, Jingjing
He, Dong
Xiao, Mengqing
Xiang, Liang
Jin, Long
Zhou, Jianda
Gong, Lian
Zhou, Yanhong
Zhou, Ming
Xiong, Wei
Xing, Xiaowei
Li, Ruhong
Cao, Ke
author_sort Zhu, Yuxing
collection PubMed
description Background: Long non-coding RNAs (LncRNAs) have been associated with several types of cancer. However, little is known about their role in lung adenocarcinoma (LUAD). Results: LINC00968 was significantly differentially expressed in LUAD tissues. Downregulated LINC00968 was associated with clinicopathological features of LUAD. LINC00968 inhibited cell growth and metastasis by regulating the Hippo signaling pathway We demonstrated that LINC00968 acts as a ceRNA to consume miR-21-5p, enhancing the accumulation of SMAD7, a miR-21-5p target. Conclusions: LINC00968 limits LUAD progression via the miR-21-5p/SMAD7 axis and may serve as a prognostic biomarker and therapeutic target for LUAD. Methods: We conducted comprehensive data mining on LINC00968 based on the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) database. The expression of LINC00968 in LUAD cells was determined using in situ hybridization. We detected LINC00968 function in LUAD cells using the MTT, clone formation, and transwell assays, and tumor xenografts. Label-free quantitative proteomics, western blotting, a dual-luciferase reporter assay, immunofluorescence, and RNA immunoprecipitation assays were used to determine the correlations among LINC00968, miR-21-5p, and SMAD7. Gain- and loss-function approaches were used to explore the effects of LINC00968, miR-21-5p, and SMAD7 on cell proliferation, migration, and invasion.
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spelling pubmed-76953982020-12-04 LINC00968 can inhibit the progression of lung adenocarcinoma through the miR-21-5p/SMAD7 signal axis Zhu, Yuxing Bo, Hao Chen, Zhizhao Li, Jingjing He, Dong Xiao, Mengqing Xiang, Liang Jin, Long Zhou, Jianda Gong, Lian Zhou, Yanhong Zhou, Ming Xiong, Wei Xing, Xiaowei Li, Ruhong Cao, Ke Aging (Albany NY) Research Paper Background: Long non-coding RNAs (LncRNAs) have been associated with several types of cancer. However, little is known about their role in lung adenocarcinoma (LUAD). Results: LINC00968 was significantly differentially expressed in LUAD tissues. Downregulated LINC00968 was associated with clinicopathological features of LUAD. LINC00968 inhibited cell growth and metastasis by regulating the Hippo signaling pathway We demonstrated that LINC00968 acts as a ceRNA to consume miR-21-5p, enhancing the accumulation of SMAD7, a miR-21-5p target. Conclusions: LINC00968 limits LUAD progression via the miR-21-5p/SMAD7 axis and may serve as a prognostic biomarker and therapeutic target for LUAD. Methods: We conducted comprehensive data mining on LINC00968 based on the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) database. The expression of LINC00968 in LUAD cells was determined using in situ hybridization. We detected LINC00968 function in LUAD cells using the MTT, clone formation, and transwell assays, and tumor xenografts. Label-free quantitative proteomics, western blotting, a dual-luciferase reporter assay, immunofluorescence, and RNA immunoprecipitation assays were used to determine the correlations among LINC00968, miR-21-5p, and SMAD7. Gain- and loss-function approaches were used to explore the effects of LINC00968, miR-21-5p, and SMAD7 on cell proliferation, migration, and invasion. Impact Journals 2020-11-04 /pmc/articles/PMC7695398/ /pubmed/33147570 http://dx.doi.org/10.18632/aging.104011 Text en Copyright: © 2020 Li et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/3.0/) (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Zhu, Yuxing
Bo, Hao
Chen, Zhizhao
Li, Jingjing
He, Dong
Xiao, Mengqing
Xiang, Liang
Jin, Long
Zhou, Jianda
Gong, Lian
Zhou, Yanhong
Zhou, Ming
Xiong, Wei
Xing, Xiaowei
Li, Ruhong
Cao, Ke
LINC00968 can inhibit the progression of lung adenocarcinoma through the miR-21-5p/SMAD7 signal axis
title LINC00968 can inhibit the progression of lung adenocarcinoma through the miR-21-5p/SMAD7 signal axis
title_full LINC00968 can inhibit the progression of lung adenocarcinoma through the miR-21-5p/SMAD7 signal axis
title_fullStr LINC00968 can inhibit the progression of lung adenocarcinoma through the miR-21-5p/SMAD7 signal axis
title_full_unstemmed LINC00968 can inhibit the progression of lung adenocarcinoma through the miR-21-5p/SMAD7 signal axis
title_short LINC00968 can inhibit the progression of lung adenocarcinoma through the miR-21-5p/SMAD7 signal axis
title_sort linc00968 can inhibit the progression of lung adenocarcinoma through the mir-21-5p/smad7 signal axis
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7695398/
https://www.ncbi.nlm.nih.gov/pubmed/33147570
http://dx.doi.org/10.18632/aging.104011
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