Cargando…

SP1-Induced Upregulation of lncRNA LINC00659 Promotes Tumour Progression in Gastric Cancer by Regulating miR-370/AQP3 Axis

Growing evidence demonstrates that long noncoding RNAs (lncRNAs) play critical roles in various human tumors. LncRNA LINC00659 (LINC00659) is a newly identified lncRNA and its roles in tumors remain largely unclear. In this study, we elucidated the potential functions and molecular mechanisms of LIN...

Descripción completa

Detalles Bibliográficos
Autores principales: Wang, Yao, Guo, Yuanyuan, Zhuang, Tianchi, Xu, Ting, Ji, Minghui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9361049/
https://www.ncbi.nlm.nih.gov/pubmed/35957833
http://dx.doi.org/10.3389/fendo.2022.936037
_version_ 1784764446429675520
author Wang, Yao
Guo, Yuanyuan
Zhuang, Tianchi
Xu, Ting
Ji, Minghui
author_facet Wang, Yao
Guo, Yuanyuan
Zhuang, Tianchi
Xu, Ting
Ji, Minghui
author_sort Wang, Yao
collection PubMed
description Growing evidence demonstrates that long noncoding RNAs (lncRNAs) play critical roles in various human tumors. LncRNA LINC00659 (LINC00659) is a newly identified lncRNA and its roles in tumors remain largely unclear. In this study, we elucidated the potential functions and molecular mechanisms of LINC00659 on the biological behaviors of gastric cancer (GC), and also explored its clinical significance. We firstly demonstrated that LINC00659 levels were distinctly up-regulated in both GC specimens and cells using bioinformatics analysis and RT-PCR. The results of ChIP assays and luciferase reporter assays confirmed that upregulation of LINC00659 was activated by SP1 in GC. Clinical assays revealed that higher levels of LINC00659 were associated with TNM stage, lymphatic metastasis, and poorer prognosis. Moreover, LINC00659 was confirmed to be an independent prognostic marker for the patients with GC using multivariate assays. Lost-of-function assays indicated that knockdown of LINC00659 suppressed the proliferation, metastasis, and EMT progress of GC cells in vitro. Mechanistic investigation indicated that LINC00659 served as a competing endogenous RNA (ceRNA) for miR-370, thereby resulting in the upregulation of leading to the depression of its endogenous target gene AQP3. Overall, our present study revealed that the LINC00659/miR-370/AQP3 axis contributes to GC progression, which may provide clues for the exploration of cancer biomarkers and therapeutic targets for GC.
format Online
Article
Text
id pubmed-9361049
institution National Center for Biotechnology Information
language English
publishDate 2022
publisher Frontiers Media S.A.
record_format MEDLINE/PubMed
spelling pubmed-93610492022-08-10 SP1-Induced Upregulation of lncRNA LINC00659 Promotes Tumour Progression in Gastric Cancer by Regulating miR-370/AQP3 Axis Wang, Yao Guo, Yuanyuan Zhuang, Tianchi Xu, Ting Ji, Minghui Front Endocrinol (Lausanne) Endocrinology Growing evidence demonstrates that long noncoding RNAs (lncRNAs) play critical roles in various human tumors. LncRNA LINC00659 (LINC00659) is a newly identified lncRNA and its roles in tumors remain largely unclear. In this study, we elucidated the potential functions and molecular mechanisms of LINC00659 on the biological behaviors of gastric cancer (GC), and also explored its clinical significance. We firstly demonstrated that LINC00659 levels were distinctly up-regulated in both GC specimens and cells using bioinformatics analysis and RT-PCR. The results of ChIP assays and luciferase reporter assays confirmed that upregulation of LINC00659 was activated by SP1 in GC. Clinical assays revealed that higher levels of LINC00659 were associated with TNM stage, lymphatic metastasis, and poorer prognosis. Moreover, LINC00659 was confirmed to be an independent prognostic marker for the patients with GC using multivariate assays. Lost-of-function assays indicated that knockdown of LINC00659 suppressed the proliferation, metastasis, and EMT progress of GC cells in vitro. Mechanistic investigation indicated that LINC00659 served as a competing endogenous RNA (ceRNA) for miR-370, thereby resulting in the upregulation of leading to the depression of its endogenous target gene AQP3. Overall, our present study revealed that the LINC00659/miR-370/AQP3 axis contributes to GC progression, which may provide clues for the exploration of cancer biomarkers and therapeutic targets for GC. Frontiers Media S.A. 2022-07-26 /pmc/articles/PMC9361049/ /pubmed/35957833 http://dx.doi.org/10.3389/fendo.2022.936037 Text en Copyright © 2022 Wang, Guo, Zhuang, Xu and Ji https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Endocrinology
Wang, Yao
Guo, Yuanyuan
Zhuang, Tianchi
Xu, Ting
Ji, Minghui
SP1-Induced Upregulation of lncRNA LINC00659 Promotes Tumour Progression in Gastric Cancer by Regulating miR-370/AQP3 Axis
title SP1-Induced Upregulation of lncRNA LINC00659 Promotes Tumour Progression in Gastric Cancer by Regulating miR-370/AQP3 Axis
title_full SP1-Induced Upregulation of lncRNA LINC00659 Promotes Tumour Progression in Gastric Cancer by Regulating miR-370/AQP3 Axis
title_fullStr SP1-Induced Upregulation of lncRNA LINC00659 Promotes Tumour Progression in Gastric Cancer by Regulating miR-370/AQP3 Axis
title_full_unstemmed SP1-Induced Upregulation of lncRNA LINC00659 Promotes Tumour Progression in Gastric Cancer by Regulating miR-370/AQP3 Axis
title_short SP1-Induced Upregulation of lncRNA LINC00659 Promotes Tumour Progression in Gastric Cancer by Regulating miR-370/AQP3 Axis
title_sort sp1-induced upregulation of lncrna linc00659 promotes tumour progression in gastric cancer by regulating mir-370/aqp3 axis
topic Endocrinology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9361049/
https://www.ncbi.nlm.nih.gov/pubmed/35957833
http://dx.doi.org/10.3389/fendo.2022.936037
work_keys_str_mv AT wangyao sp1inducedupregulationoflncrnalinc00659promotestumourprogressioningastriccancerbyregulatingmir370aqp3axis
AT guoyuanyuan sp1inducedupregulationoflncrnalinc00659promotestumourprogressioningastriccancerbyregulatingmir370aqp3axis
AT zhuangtianchi sp1inducedupregulationoflncrnalinc00659promotestumourprogressioningastriccancerbyregulatingmir370aqp3axis
AT xuting sp1inducedupregulationoflncrnalinc00659promotestumourprogressioningastriccancerbyregulatingmir370aqp3axis
AT jiminghui sp1inducedupregulationoflncrnalinc00659promotestumourprogressioningastriccancerbyregulatingmir370aqp3axis