FOXP1 inhibits pancreatic cancer growth by transcriptionally regulating IRF1 expression

FOXP1, known as a Forkhead-box (FOX) family protein, plays an important role in human tumorigenesis. However, the function and molecular mechanism of FOXP1 in pancreatic cancer (PC) remain unclear. Here, we report that PC patients with FOXP1 overexpression had a higher survival rate compared to pati...

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Autores principales: Wang, Le, Luo, Ping, Yang, Zhiwen, Zhong, Xiaoming, Ji, Changxue
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2023
Materias:
Research Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10035899/
https://www.ncbi.nlm.nih.gov/pubmed/36952469
http://dx.doi.org/10.1371/journal.pone.0280794
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author Wang, Le
Luo, Ping
Yang, Zhiwen
Zhong, Xiaoming
Ji, Changxue
author_facet Wang, Le
Luo, Ping
Yang, Zhiwen
Zhong, Xiaoming
Ji, Changxue
author_sort Wang, Le
collection PubMed
description FOXP1, known as a Forkhead-box (FOX) family protein, plays an important role in human tumorigenesis. However, the function and molecular mechanism of FOXP1 in pancreatic cancer (PC) remain unclear. Here, we report that PC patients with FOXP1 overexpression had a higher survival rate compared to patients with low- FOXP1 expression. Additionally, high expression of FOXP1 can markedly inhibit the growth of pancreatic cancer in vivo and in vitro, whereas low expression of FOXP1 effectively promoted the tumorigenesis. Mechanistically, FOXP1 could directly bind the IRF1 promoter, which triggered the transcriptional activity of IRF1. Taken together, FOXP1 suppressed PC growth via IRF1-dependent manner, serving as a potential prognostic biomarker for patients with PC.
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spelling pubmed-100358992023-03-24 FOXP1 inhibits pancreatic cancer growth by transcriptionally regulating IRF1 expression Wang, Le Luo, Ping Yang, Zhiwen Zhong, Xiaoming Ji, Changxue PLoS One Research Article FOXP1, known as a Forkhead-box (FOX) family protein, plays an important role in human tumorigenesis. However, the function and molecular mechanism of FOXP1 in pancreatic cancer (PC) remain unclear. Here, we report that PC patients with FOXP1 overexpression had a higher survival rate compared to patients with low- FOXP1 expression. Additionally, high expression of FOXP1 can markedly inhibit the growth of pancreatic cancer in vivo and in vitro, whereas low expression of FOXP1 effectively promoted the tumorigenesis. Mechanistically, FOXP1 could directly bind the IRF1 promoter, which triggered the transcriptional activity of IRF1. Taken together, FOXP1 suppressed PC growth via IRF1-dependent manner, serving as a potential prognostic biomarker for patients with PC. Public Library of Science 2023-03-23 /pmc/articles/PMC10035899/ /pubmed/36952469 http://dx.doi.org/10.1371/journal.pone.0280794 Text en © 2023 Wang et al https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Wang, Le
Luo, Ping
Yang, Zhiwen
Zhong, Xiaoming
Ji, Changxue
FOXP1 inhibits pancreatic cancer growth by transcriptionally regulating IRF1 expression
title FOXP1 inhibits pancreatic cancer growth by transcriptionally regulating IRF1 expression
title_full FOXP1 inhibits pancreatic cancer growth by transcriptionally regulating IRF1 expression
title_fullStr FOXP1 inhibits pancreatic cancer growth by transcriptionally regulating IRF1 expression
title_full_unstemmed FOXP1 inhibits pancreatic cancer growth by transcriptionally regulating IRF1 expression
title_short FOXP1 inhibits pancreatic cancer growth by transcriptionally regulating IRF1 expression
title_sort foxp1 inhibits pancreatic cancer growth by transcriptionally regulating irf1 expression
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10035899/
https://www.ncbi.nlm.nih.gov/pubmed/36952469
http://dx.doi.org/10.1371/journal.pone.0280794
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