ArticleTranslational cancer research2021
Up-regulation of SOCS4 promotes cell proliferation and migration in esophageal squamous cell carcinoma.
Article in Translational cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- The Neglected Suppressor of Cytokine Signalling (SOCS): SOCS4-7.Inflammation · 2025Review
- MiR-568-5p, the key regulator of suppressor of cytokine signaling 4 (SOCS4) in the coronary artery disease.Journal of diabetes and metabolic disorders · 2025Article
- Expression Characteristics, Immune Signature, and Prognostic Value of the SOCS Family Identified by Multiomics Integrative Analysis in Liver Cancer.Cancer reports (Hoboken, N.J.) · 2024Article
- SPP1 promotes tumor progression in esophageal carcinoma by activating focal adhesion pathway.Journal of gastrointestinal oncology · 2024Article
- Bufalin suppresses esophageal squamous cell carcinoma progression by activating the PIAS3/STAT3 signaling pathway.Journal of thoracic disease · 2023Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSuppressors of cytokine signaling family member 4 (SOCS4) was shown to serve critical and multifaceted roles in the progression of numerous cancers, including hepatocellular carcinoma, thyroid cancer, breast cancer, and lung adenocarcinoma. While, the expression and the roles of SOCS4 in esophageal squamous cell carcinoma (ESCC) remain elusive. The current study is aimed to investigate the expression pattern and functions of SOCS4 in ESCC.
methodsThe relationship between SOCS4 and the clinicopathological features of ESCC was analyzed. SOCS4 expression in ESCC tissues was measured by western blot, quantitative real-time polymerase chain reaction (qRT-PCR), and immunohistochemical (IHC) staining. The roles of SOCS4 in modulating ESCC cell behaviors were examined using a series of assays, including cell proliferation assay, cell counting kit-8 (CCK-8) assay, cell cycle analysis, and wound-healing assay.
resultsIn human ESCC tissues, SOCS4 expression was up-regulated and correlated with tumor size and lymph node metastasis, however was not correlated with the overall survival (OS) of patients. SOCS4 silencing in ESCC cells resulted in the suppression of cell growth, which was related to the cell cycle. SOCS4 knockdown also inhibited nuclear factor-kappa B (NF-κB) signaling and decreased the migratory potential of ESCC cells.
conclusionsThese findings revealed that increased expression of SOCS4 in ESCC may promote the progression, proliferation, and migration by NF-κB signaling. Inhibition of SOCS4 may be a promising therapeutic strategy for ESCC.
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