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Comprehensive analysis of suppressor of cytokine signaling 2 protein in the malignant transformation of NSCLC
Suppressor of cytokine signaling 2 (SOCS2) plays an essential role in a number of physiological phenomena and functions as a tumor suppressor. Understanding the predictive effects of SOCS2 on non-small cell lung cancer (NSCLC) is urgently needed. The Cancer Genome Atlas (TCGA) and Gene Expression Om...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2023
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10320659/ https://www.ncbi.nlm.nih.gov/pubmed/37415839 http://dx.doi.org/10.3892/etm.2023.12069 |
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author | Ma, Guoyuan Zeng, Yukai Zhong, Weiqing Zhao, Xiaogang Wang, Guanghui Bie, Fenglong Du, Jiajun |
author_facet | Ma, Guoyuan Zeng, Yukai Zhong, Weiqing Zhao, Xiaogang Wang, Guanghui Bie, Fenglong Du, Jiajun |
author_sort | Ma, Guoyuan |
collection | PubMed |
description | Suppressor of cytokine signaling 2 (SOCS2) plays an essential role in a number of physiological phenomena and functions as a tumor suppressor. Understanding the predictive effects of SOCS2 on non-small cell lung cancer (NSCLC) is urgently needed. The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases were used to assess SOCS2 gene expression levels in NSCLC. The clinical significance of SOCS2 was evaluated through Kaplan-Meier curve analysis and the analysis of related clinical factors. Gene Set Enrichment Analysis (GSEA) was used to identify the biological functions of SOCS2. Subsequently proliferation, wound-healing, colony formation and Transwell assays, and carboplatin drug experiments were used for verification. The results revealed that SOCS2 expression was low in the NSCLC tissues of patients in TCGA and GEO database analyses. Downregulated SOCS2 was associated with poor prognosis, as determined by Kaplan-Meier survival analysis (HR 0.61, 95% CI 0.52-0.73; P<0.001). GSEA showed that SOCS2 was involved in intracellular reactions, including epithelial-mesenchymal transition (EMT). Cell experiments indicated that knockdown of SOCS2 caused the malignant progression of NSCLC cell lines. Furthermore, the drug experiment showed that silencing of SOCS2 promoted the resistance of NSCLC cells to carboplatin. In conclusion, low expression of SOCS2 was associated with poor clinical prognosis by effecting EMT and causing drug resistance in NSCLC cell lines. Furthermore, SOCS2 could act as a predictive indicator for NSCLC. |
format | Online Article Text |
id | pubmed-10320659 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-103206592023-07-06 Comprehensive analysis of suppressor of cytokine signaling 2 protein in the malignant transformation of NSCLC Ma, Guoyuan Zeng, Yukai Zhong, Weiqing Zhao, Xiaogang Wang, Guanghui Bie, Fenglong Du, Jiajun Exp Ther Med Articles Suppressor of cytokine signaling 2 (SOCS2) plays an essential role in a number of physiological phenomena and functions as a tumor suppressor. Understanding the predictive effects of SOCS2 on non-small cell lung cancer (NSCLC) is urgently needed. The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases were used to assess SOCS2 gene expression levels in NSCLC. The clinical significance of SOCS2 was evaluated through Kaplan-Meier curve analysis and the analysis of related clinical factors. Gene Set Enrichment Analysis (GSEA) was used to identify the biological functions of SOCS2. Subsequently proliferation, wound-healing, colony formation and Transwell assays, and carboplatin drug experiments were used for verification. The results revealed that SOCS2 expression was low in the NSCLC tissues of patients in TCGA and GEO database analyses. Downregulated SOCS2 was associated with poor prognosis, as determined by Kaplan-Meier survival analysis (HR 0.61, 95% CI 0.52-0.73; P<0.001). GSEA showed that SOCS2 was involved in intracellular reactions, including epithelial-mesenchymal transition (EMT). Cell experiments indicated that knockdown of SOCS2 caused the malignant progression of NSCLC cell lines. Furthermore, the drug experiment showed that silencing of SOCS2 promoted the resistance of NSCLC cells to carboplatin. In conclusion, low expression of SOCS2 was associated with poor clinical prognosis by effecting EMT and causing drug resistance in NSCLC cell lines. Furthermore, SOCS2 could act as a predictive indicator for NSCLC. D.A. Spandidos 2023-06-19 /pmc/articles/PMC10320659/ /pubmed/37415839 http://dx.doi.org/10.3892/etm.2023.12069 Text en Copyright: © Ma et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Ma, Guoyuan Zeng, Yukai Zhong, Weiqing Zhao, Xiaogang Wang, Guanghui Bie, Fenglong Du, Jiajun Comprehensive analysis of suppressor of cytokine signaling 2 protein in the malignant transformation of NSCLC |
title | Comprehensive analysis of suppressor of cytokine signaling 2 protein in the malignant transformation of NSCLC |
title_full | Comprehensive analysis of suppressor of cytokine signaling 2 protein in the malignant transformation of NSCLC |
title_fullStr | Comprehensive analysis of suppressor of cytokine signaling 2 protein in the malignant transformation of NSCLC |
title_full_unstemmed | Comprehensive analysis of suppressor of cytokine signaling 2 protein in the malignant transformation of NSCLC |
title_short | Comprehensive analysis of suppressor of cytokine signaling 2 protein in the malignant transformation of NSCLC |
title_sort | comprehensive analysis of suppressor of cytokine signaling 2 protein in the malignant transformation of nsclc |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10320659/ https://www.ncbi.nlm.nih.gov/pubmed/37415839 http://dx.doi.org/10.3892/etm.2023.12069 |
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