ArticleExperimental and therapeutic medicine2023
Comprehensive analysis of suppressor of cytokine signaling 2 protein in the malignant transformation of NSCLC.
Article in Experimental and therapeutic medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 2 citations in OpenAlex.
- SIRT6 cooperates with KDM5C to transcriptionally silence MICAL2 and inhibit tumorigenesis in pancreatic cancer.Cell communication and signaling : CCS · 2026Article
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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