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Regulation of follistatin-like 3 expression by miR-486-5p modulates gastric cancer cell proliferation, migration and tumor progression

Cancer development and progression can be regulated by the levels of endogenous factors. Gastric cancer is an aggressive disease state with poor patient prognosis, needing the development of new diagnostics and therapeutic strategies. We investigated the close association between follistatin-like 3...

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Autores principales: Dai, Zhou-Tong, Xiang, Yuan, Zhang, Xiao-Yu, Zong, Qi-Bei, Wu, Qi-Fang, Huang, You, Shen, Chao, Li, Jia-Peng, Ponnambalam, Sreenivasan, Liao, Xing-Hua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8436905/
https://www.ncbi.nlm.nih.gov/pubmed/34425560
http://dx.doi.org/10.18632/aging.203412
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author Dai, Zhou-Tong
Xiang, Yuan
Zhang, Xiao-Yu
Zong, Qi-Bei
Wu, Qi-Fang
Huang, You
Shen, Chao
Li, Jia-Peng
Ponnambalam, Sreenivasan
Liao, Xing-Hua
author_facet Dai, Zhou-Tong
Xiang, Yuan
Zhang, Xiao-Yu
Zong, Qi-Bei
Wu, Qi-Fang
Huang, You
Shen, Chao
Li, Jia-Peng
Ponnambalam, Sreenivasan
Liao, Xing-Hua
author_sort Dai, Zhou-Tong
collection PubMed
description Cancer development and progression can be regulated by the levels of endogenous factors. Gastric cancer is an aggressive disease state with poor patient prognosis, needing the development of new diagnostics and therapeutic strategies. We investigated the close association between follistatin-like 3 (FSTL3) and different cancers, and focused on its role in gastric cancer cell function. Using cancer bioinformatics, we found that FSTL3 expression is elevated in a large majority of the 33 cancers we analyzed in publicly available cancer databases. Elevated levels of FSTL3 is associated with poor patient prognosis in gastric cancer. In a comparison of normal gastric epithelial cells and gastric cancer cell lines, FSTL3 expression was consistently elevated in gastric cancer cells. Overexpression of FSTL3 promoted gastric cancer cell viability, proliferation and migration. Conversely, FSTL3 knockdown inhibits these cellular processes. Using bioinformatics, we found that the FSTL3 mRNA has a potential binding site in the 3’-UTR for a small microRNA, miR-486-5p. Further bioinformatics revealed significant negative correlation between FSTL3 and miR-486-5p levels. Using luciferase reporter constructs, we provide evidence that the 3’UTR from the FSTL3 mRNA can confer downregulation in the presence of miR-486-5p. These studies lead us to conclude that FSTL3 has oncogenic properties and increased expression of this gene product promotes gastric cancer development and progression.
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spelling pubmed-84369052021-09-14 Regulation of follistatin-like 3 expression by miR-486-5p modulates gastric cancer cell proliferation, migration and tumor progression Dai, Zhou-Tong Xiang, Yuan Zhang, Xiao-Yu Zong, Qi-Bei Wu, Qi-Fang Huang, You Shen, Chao Li, Jia-Peng Ponnambalam, Sreenivasan Liao, Xing-Hua Aging (Albany NY) Research Paper Cancer development and progression can be regulated by the levels of endogenous factors. Gastric cancer is an aggressive disease state with poor patient prognosis, needing the development of new diagnostics and therapeutic strategies. We investigated the close association between follistatin-like 3 (FSTL3) and different cancers, and focused on its role in gastric cancer cell function. Using cancer bioinformatics, we found that FSTL3 expression is elevated in a large majority of the 33 cancers we analyzed in publicly available cancer databases. Elevated levels of FSTL3 is associated with poor patient prognosis in gastric cancer. In a comparison of normal gastric epithelial cells and gastric cancer cell lines, FSTL3 expression was consistently elevated in gastric cancer cells. Overexpression of FSTL3 promoted gastric cancer cell viability, proliferation and migration. Conversely, FSTL3 knockdown inhibits these cellular processes. Using bioinformatics, we found that the FSTL3 mRNA has a potential binding site in the 3’-UTR for a small microRNA, miR-486-5p. Further bioinformatics revealed significant negative correlation between FSTL3 and miR-486-5p levels. Using luciferase reporter constructs, we provide evidence that the 3’UTR from the FSTL3 mRNA can confer downregulation in the presence of miR-486-5p. These studies lead us to conclude that FSTL3 has oncogenic properties and increased expression of this gene product promotes gastric cancer development and progression. Impact Journals 2021-08-23 /pmc/articles/PMC8436905/ /pubmed/34425560 http://dx.doi.org/10.18632/aging.203412 Text en Copyright: © 2021 Dai 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
Dai, Zhou-Tong
Xiang, Yuan
Zhang, Xiao-Yu
Zong, Qi-Bei
Wu, Qi-Fang
Huang, You
Shen, Chao
Li, Jia-Peng
Ponnambalam, Sreenivasan
Liao, Xing-Hua
Regulation of follistatin-like 3 expression by miR-486-5p modulates gastric cancer cell proliferation, migration and tumor progression
title Regulation of follistatin-like 3 expression by miR-486-5p modulates gastric cancer cell proliferation, migration and tumor progression
title_full Regulation of follistatin-like 3 expression by miR-486-5p modulates gastric cancer cell proliferation, migration and tumor progression
title_fullStr Regulation of follistatin-like 3 expression by miR-486-5p modulates gastric cancer cell proliferation, migration and tumor progression
title_full_unstemmed Regulation of follistatin-like 3 expression by miR-486-5p modulates gastric cancer cell proliferation, migration and tumor progression
title_short Regulation of follistatin-like 3 expression by miR-486-5p modulates gastric cancer cell proliferation, migration and tumor progression
title_sort regulation of follistatin-like 3 expression by mir-486-5p modulates gastric cancer cell proliferation, migration and tumor progression
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8436905/
https://www.ncbi.nlm.nih.gov/pubmed/34425560
http://dx.doi.org/10.18632/aging.203412
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