Transcription factor KLF15 inhibits the proliferation and migration of gastric cancer cells via regulating the TFAP2A-AS1/NISCH axis

Abstract Background Recently, overwhelming evidence supports that long noncoding RNAs (lncRNAs) play crucial roles in the occurrence and progression of tumors. However, the role and mechanism of lncRNA TFAP2A-AS1 in human gastric cancer (GC) remains unclear. Thus, the biological role and regulatory...

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Autores principales:	Xin Zhao, Linlin Chen, Jingxun Wu, Jun You, Qingqi Hong, Feng Ye
Formato:	article
Lenguaje:	EN
Publicado:	BMC 2021
Materias:	KLF15 TFAP2A-AS1 NISCH Gastric cancer (GC) Transcription factor Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/c3c1aabdf9494354b22566e903d3afae
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spelling	oai:doaj.org-article:c3c1aabdf9494354b22566e903d3afae2021-11-07T12:08:40ZTranscription factor KLF15 inhibits the proliferation and migration of gastric cancer cells via regulating the TFAP2A-AS1/NISCH axis10.1186/s13062-021-00300-y1745-6150https://doaj.org/article/c3c1aabdf9494354b22566e903d3afae2021-11-01T00:00:00Zhttps://doi.org/10.1186/s13062-021-00300-yhttps://doaj.org/toc/1745-6150Abstract Background Recently, overwhelming evidence supports that long noncoding RNAs (lncRNAs) play crucial roles in the occurrence and progression of tumors. However, the role and mechanism of lncRNA TFAP2A-AS1 in human gastric cancer (GC) remains unclear. Thus, the biological role and regulatory mechanisms of TFAP2A-AS1 in GC were explored. Methods Quantitative real-time PCR (qPCR) was applied to detect gene expression. Western blot was used to measure protein expression. Cell proliferation and migration were determined by functional assays. Fluorescence in situ hybridization (FISH) assays were performed to determine the subcellular distribution of TFAP2A-AS1 in GC. Mechanism investigations were conducted to explore the downstream genes of TFAP2A-AS1 and the upstream transcription factor of TFAP2A-AS1 in GC cells. Results TFAP2A-AS1 inhibits the proliferation and migration of GC cells. In the downstream regulation mechanism, miR-3657 was verified as the downstream gene of TFAP2A-AS1 and NISCH as the target of miR-3657. NISCH also suppresses cell proliferation and migration in GC. In the upstream regulation mechanism, transcription factor KLF15 positively mediates TFAP2A-AS1 to suppress GC cell proliferation and migration. Conclusion KLF15-mediated TFAP2A-AS1 hampers cell proliferation and migration in GC via miR-3657/NISCH axis.Xin ZhaoLinlin ChenJingxun WuJun YouQingqi HongFeng YeBMCarticleKLF15TFAP2A-AS1NISCHGastric cancer (GC)Transcription factorBiology (General)QH301-705.5ENBiology Direct, Vol 16, Iss 1, Pp 1-11 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	KLF15 TFAP2A-AS1 NISCH Gastric cancer (GC) Transcription factor Biology (General) QH301-705.5
spellingShingle	KLF15 TFAP2A-AS1 NISCH Gastric cancer (GC) Transcription factor Biology (General) QH301-705.5 Xin Zhao Linlin Chen Jingxun Wu Jun You Qingqi Hong Feng Ye Transcription factor KLF15 inhibits the proliferation and migration of gastric cancer cells via regulating the TFAP2A-AS1/NISCH axis
description	Abstract Background Recently, overwhelming evidence supports that long noncoding RNAs (lncRNAs) play crucial roles in the occurrence and progression of tumors. However, the role and mechanism of lncRNA TFAP2A-AS1 in human gastric cancer (GC) remains unclear. Thus, the biological role and regulatory mechanisms of TFAP2A-AS1 in GC were explored. Methods Quantitative real-time PCR (qPCR) was applied to detect gene expression. Western blot was used to measure protein expression. Cell proliferation and migration were determined by functional assays. Fluorescence in situ hybridization (FISH) assays were performed to determine the subcellular distribution of TFAP2A-AS1 in GC. Mechanism investigations were conducted to explore the downstream genes of TFAP2A-AS1 and the upstream transcription factor of TFAP2A-AS1 in GC cells. Results TFAP2A-AS1 inhibits the proliferation and migration of GC cells. In the downstream regulation mechanism, miR-3657 was verified as the downstream gene of TFAP2A-AS1 and NISCH as the target of miR-3657. NISCH also suppresses cell proliferation and migration in GC. In the upstream regulation mechanism, transcription factor KLF15 positively mediates TFAP2A-AS1 to suppress GC cell proliferation and migration. Conclusion KLF15-mediated TFAP2A-AS1 hampers cell proliferation and migration in GC via miR-3657/NISCH axis.
format	article
author	Xin Zhao Linlin Chen Jingxun Wu Jun You Qingqi Hong Feng Ye
author_facet	Xin Zhao Linlin Chen Jingxun Wu Jun You Qingqi Hong Feng Ye
author_sort	Xin Zhao
title	Transcription factor KLF15 inhibits the proliferation and migration of gastric cancer cells via regulating the TFAP2A-AS1/NISCH axis
title_short	Transcription factor KLF15 inhibits the proliferation and migration of gastric cancer cells via regulating the TFAP2A-AS1/NISCH axis
title_full	Transcription factor KLF15 inhibits the proliferation and migration of gastric cancer cells via regulating the TFAP2A-AS1/NISCH axis
title_fullStr	Transcription factor KLF15 inhibits the proliferation and migration of gastric cancer cells via regulating the TFAP2A-AS1/NISCH axis
title_full_unstemmed	Transcription factor KLF15 inhibits the proliferation and migration of gastric cancer cells via regulating the TFAP2A-AS1/NISCH axis
title_sort	transcription factor klf15 inhibits the proliferation and migration of gastric cancer cells via regulating the tfap2a-as1/nisch axis
publisher	BMC
publishDate	2021
url	https://doaj.org/article/c3c1aabdf9494354b22566e903d3afae
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Transcription factor KLF15 inhibits the proliferation and migration of gastric cancer cells via regulating the TFAP2A-AS1/NISCH axis

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