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TGIF1 overexpression promotes glioma progression and worsens patient prognosis

Transforming growth factor β‐induced factor homeobox 1 (TGIF1) reportedly promotes the pathological processes of various malignant tumors. However, few studies have investigated the role of TGIF1 in gliomas. We aimed to explore the relationship between TGIF1 expression and the clinical characteristi...

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Autores principales: Wang, Baoya, Ma, Qiong, Wang, Xuelin, Guo, Kunshan, Liu, Zhendong, Li, Gang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9761070/
https://www.ncbi.nlm.nih.gov/pubmed/35569122
http://dx.doi.org/10.1002/cam4.4822
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author Wang, Baoya
Ma, Qiong
Wang, Xuelin
Guo, Kunshan
Liu, Zhendong
Li, Gang
author_facet Wang, Baoya
Ma, Qiong
Wang, Xuelin
Guo, Kunshan
Liu, Zhendong
Li, Gang
author_sort Wang, Baoya
collection PubMed
description Transforming growth factor β‐induced factor homeobox 1 (TGIF1) reportedly promotes the pathological processes of various malignant tumors. However, few studies have investigated the role of TGIF1 in gliomas. We aimed to explore the relationship between TGIF1 expression and the clinical characteristics of patients with glioma, including their overall survival. A total of thousands transcriptome datapoints were downloaded from public databases to determine the correlations between TGIF1 and various clinicopathological features using the Wilcoxon or Kruskal–Wallis tests. The Kaplan–Meier and Cox statistical methods were used to explore the prognostic significance of TGIF1. Gene set enrichment analysis (GSEA) was used to indirectly identify the pathological mechanisms modulated by TGIF1, and compounds that inhibit its expression were determined using a connectivity map (CMap). TGIF1 was significantly overexpressed in gliomas and was correlated with unfavorable prognostic factors and shorter overall survival. Cox analysis confirmed that TGIF1 expression was a significant predictor of poor prognosis in patients with glioma. GSEA revealed that the signaling pathways associated with TGIF1 expression in glioma included extracellular matrix receptor‐ and cell cycle‐modulating proteins. CMap analysis showed that the small molecules scriptaid, torasemide, dexpropranolol, ipratropium bromide, and harmine were potential negative regulators of TGIF1. Finally, in vitro experiments demonstrated that knockdown of TGIF1 significantly inhibited the proliferation and invasion of glioma cell. Taken together, our study, which is the first to comprehensively analyze TGIF1 in gliomas, revealed it to be a novel oncogene in terms of its association with this disease. As such, TGIF1 may be a potential therapeutic target for individualized treatment of patients with glioma.
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spelling pubmed-97610702022-12-20 TGIF1 overexpression promotes glioma progression and worsens patient prognosis Wang, Baoya Ma, Qiong Wang, Xuelin Guo, Kunshan Liu, Zhendong Li, Gang Cancer Med Research Articles Transforming growth factor β‐induced factor homeobox 1 (TGIF1) reportedly promotes the pathological processes of various malignant tumors. However, few studies have investigated the role of TGIF1 in gliomas. We aimed to explore the relationship between TGIF1 expression and the clinical characteristics of patients with glioma, including their overall survival. A total of thousands transcriptome datapoints were downloaded from public databases to determine the correlations between TGIF1 and various clinicopathological features using the Wilcoxon or Kruskal–Wallis tests. The Kaplan–Meier and Cox statistical methods were used to explore the prognostic significance of TGIF1. Gene set enrichment analysis (GSEA) was used to indirectly identify the pathological mechanisms modulated by TGIF1, and compounds that inhibit its expression were determined using a connectivity map (CMap). TGIF1 was significantly overexpressed in gliomas and was correlated with unfavorable prognostic factors and shorter overall survival. Cox analysis confirmed that TGIF1 expression was a significant predictor of poor prognosis in patients with glioma. GSEA revealed that the signaling pathways associated with TGIF1 expression in glioma included extracellular matrix receptor‐ and cell cycle‐modulating proteins. CMap analysis showed that the small molecules scriptaid, torasemide, dexpropranolol, ipratropium bromide, and harmine were potential negative regulators of TGIF1. Finally, in vitro experiments demonstrated that knockdown of TGIF1 significantly inhibited the proliferation and invasion of glioma cell. Taken together, our study, which is the first to comprehensively analyze TGIF1 in gliomas, revealed it to be a novel oncogene in terms of its association with this disease. As such, TGIF1 may be a potential therapeutic target for individualized treatment of patients with glioma. John Wiley and Sons Inc. 2022-05-15 /pmc/articles/PMC9761070/ /pubmed/35569122 http://dx.doi.org/10.1002/cam4.4822 Text en © 2022 The Authors. Cancer Medicine published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Articles
Wang, Baoya
Ma, Qiong
Wang, Xuelin
Guo, Kunshan
Liu, Zhendong
Li, Gang
TGIF1 overexpression promotes glioma progression and worsens patient prognosis
title TGIF1 overexpression promotes glioma progression and worsens patient prognosis
title_full TGIF1 overexpression promotes glioma progression and worsens patient prognosis
title_fullStr TGIF1 overexpression promotes glioma progression and worsens patient prognosis
title_full_unstemmed TGIF1 overexpression promotes glioma progression and worsens patient prognosis
title_short TGIF1 overexpression promotes glioma progression and worsens patient prognosis
title_sort tgif1 overexpression promotes glioma progression and worsens patient prognosis
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9761070/
https://www.ncbi.nlm.nih.gov/pubmed/35569122
http://dx.doi.org/10.1002/cam4.4822
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