Cargando…
LINC00853 contributes to tumor stemness of gastric cancer through FOXP3-mediated transcription of PDZK1IP1
BACKGROUND: The incidence and mortality of gastric cancer (GC) are high worldwide. Tumor stemness is a major contributor to tumorigenesis and development of GC, in which long non-coding RNAs (lncRNAs) are deeply involved. The purpose of this study was to investigate the influences and mechanisms of...
Autores principales: | , , , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2023
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10318836/ https://www.ncbi.nlm.nih.gov/pubmed/37403034 http://dx.doi.org/10.1186/s12575-023-00213-2 |
_version_ | 1785068127042666496 |
---|---|
author | Hu, Xia Zhao, Maoyuan Hu, Shuangyuan Liu, Qingsong Liao, Wenhao Wan, Lina Wei, Feng Su, Fangting Guo, Yu Zeng, Jinhao |
author_facet | Hu, Xia Zhao, Maoyuan Hu, Shuangyuan Liu, Qingsong Liao, Wenhao Wan, Lina Wei, Feng Su, Fangting Guo, Yu Zeng, Jinhao |
author_sort | Hu, Xia |
collection | PubMed |
description | BACKGROUND: The incidence and mortality of gastric cancer (GC) are high worldwide. Tumor stemness is a major contributor to tumorigenesis and development of GC, in which long non-coding RNAs (lncRNAs) are deeply involved. The purpose of this study was to investigate the influences and mechanisms of LINC00853 in the progression and stemness of GC. METHODS: The level of LINC00853 was assessed based on The Cancer Genome Atlas (TCGA) database and GC cell lines by RT-PCR and in situ hybridization. An evaluation of biological functions of LINC00853 including cell proliferation, migration, and tumor stemness was conducted via gain-and loss-of-function experiments. Furthermore, RNA pull-down and RNA immunoprecipitation (RIP) assay were utilized to validate the connection between LINC00853 and the transcription factor Forkhead Box P3 (FOXP3). Nude mouse xenograft model was used to identify the impacts of LINC00853 on tumor development. RESULTS: We identified the up-regulated levels of lncRNA-LINC00853 in GC, and its overexpression correlates with poor prognosis in GC patients. Further study indicated that LINC00853 promoted cell proliferation, migration and cancer stemness while suppressed cell apoptosis. Mechanistically, LINC00853 directly bind to FOXP3 and promoted FOXP3-mediated transcription of PDZK1 interacting protein 1(PDZK1IP1). Alterations of FOXP3 or PDZK1IP1 reversed the LINC00853-induced biological effects on cell proliferation, migration and stemness. Moreover, xenograft tumor assay was used to investigate the function of LINC00853 in vivo. CONCLUSIONS: Taken together, these findings revealed the tumor-promoting activity of LINC00853 in GC, expanding our understanding of lncRNAs regulation on GC pathogenesis. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12575-023-00213-2. |
format | Online Article Text |
id | pubmed-10318836 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-103188362023-07-05 LINC00853 contributes to tumor stemness of gastric cancer through FOXP3-mediated transcription of PDZK1IP1 Hu, Xia Zhao, Maoyuan Hu, Shuangyuan Liu, Qingsong Liao, Wenhao Wan, Lina Wei, Feng Su, Fangting Guo, Yu Zeng, Jinhao Biol Proced Online Research BACKGROUND: The incidence and mortality of gastric cancer (GC) are high worldwide. Tumor stemness is a major contributor to tumorigenesis and development of GC, in which long non-coding RNAs (lncRNAs) are deeply involved. The purpose of this study was to investigate the influences and mechanisms of LINC00853 in the progression and stemness of GC. METHODS: The level of LINC00853 was assessed based on The Cancer Genome Atlas (TCGA) database and GC cell lines by RT-PCR and in situ hybridization. An evaluation of biological functions of LINC00853 including cell proliferation, migration, and tumor stemness was conducted via gain-and loss-of-function experiments. Furthermore, RNA pull-down and RNA immunoprecipitation (RIP) assay were utilized to validate the connection between LINC00853 and the transcription factor Forkhead Box P3 (FOXP3). Nude mouse xenograft model was used to identify the impacts of LINC00853 on tumor development. RESULTS: We identified the up-regulated levels of lncRNA-LINC00853 in GC, and its overexpression correlates with poor prognosis in GC patients. Further study indicated that LINC00853 promoted cell proliferation, migration and cancer stemness while suppressed cell apoptosis. Mechanistically, LINC00853 directly bind to FOXP3 and promoted FOXP3-mediated transcription of PDZK1 interacting protein 1(PDZK1IP1). Alterations of FOXP3 or PDZK1IP1 reversed the LINC00853-induced biological effects on cell proliferation, migration and stemness. Moreover, xenograft tumor assay was used to investigate the function of LINC00853 in vivo. CONCLUSIONS: Taken together, these findings revealed the tumor-promoting activity of LINC00853 in GC, expanding our understanding of lncRNAs regulation on GC pathogenesis. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12575-023-00213-2. BioMed Central 2023-07-04 /pmc/articles/PMC10318836/ /pubmed/37403034 http://dx.doi.org/10.1186/s12575-023-00213-2 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Hu, Xia Zhao, Maoyuan Hu, Shuangyuan Liu, Qingsong Liao, Wenhao Wan, Lina Wei, Feng Su, Fangting Guo, Yu Zeng, Jinhao LINC00853 contributes to tumor stemness of gastric cancer through FOXP3-mediated transcription of PDZK1IP1 |
title | LINC00853 contributes to tumor stemness of gastric cancer through FOXP3-mediated transcription of PDZK1IP1 |
title_full | LINC00853 contributes to tumor stemness of gastric cancer through FOXP3-mediated transcription of PDZK1IP1 |
title_fullStr | LINC00853 contributes to tumor stemness of gastric cancer through FOXP3-mediated transcription of PDZK1IP1 |
title_full_unstemmed | LINC00853 contributes to tumor stemness of gastric cancer through FOXP3-mediated transcription of PDZK1IP1 |
title_short | LINC00853 contributes to tumor stemness of gastric cancer through FOXP3-mediated transcription of PDZK1IP1 |
title_sort | linc00853 contributes to tumor stemness of gastric cancer through foxp3-mediated transcription of pdzk1ip1 |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10318836/ https://www.ncbi.nlm.nih.gov/pubmed/37403034 http://dx.doi.org/10.1186/s12575-023-00213-2 |
work_keys_str_mv | AT huxia linc00853contributestotumorstemnessofgastriccancerthroughfoxp3mediatedtranscriptionofpdzk1ip1 AT zhaomaoyuan linc00853contributestotumorstemnessofgastriccancerthroughfoxp3mediatedtranscriptionofpdzk1ip1 AT hushuangyuan linc00853contributestotumorstemnessofgastriccancerthroughfoxp3mediatedtranscriptionofpdzk1ip1 AT liuqingsong linc00853contributestotumorstemnessofgastriccancerthroughfoxp3mediatedtranscriptionofpdzk1ip1 AT liaowenhao linc00853contributestotumorstemnessofgastriccancerthroughfoxp3mediatedtranscriptionofpdzk1ip1 AT wanlina linc00853contributestotumorstemnessofgastriccancerthroughfoxp3mediatedtranscriptionofpdzk1ip1 AT weifeng linc00853contributestotumorstemnessofgastriccancerthroughfoxp3mediatedtranscriptionofpdzk1ip1 AT sufangting linc00853contributestotumorstemnessofgastriccancerthroughfoxp3mediatedtranscriptionofpdzk1ip1 AT guoyu linc00853contributestotumorstemnessofgastriccancerthroughfoxp3mediatedtranscriptionofpdzk1ip1 AT zengjinhao linc00853contributestotumorstemnessofgastriccancerthroughfoxp3mediatedtranscriptionofpdzk1ip1 |