SOCS3 control the activity of NF-κB induced by HSP70<i>via</i>degradation of MyD88-adapter-like protein (Mal) in IPEC-J2 cells

Yong, Yanhong; Wang, Ping; RuMin, Jia; Gooneratne, Ravi; Wang, Hwa‐Chain Robert; Liao, Ming

doi:10.1080/02656736.2018.1541484

Cited by 16 publications

(14 citation statements)

References 41 publications

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“…A previous study showed that NF-κB activity was negatively regulated by SOCS4 in IPEC-J2 cells (31), which was contrary to our results. This suggested that the effect of SOCS4 on NF-κB activity depends on cell type.…”

Section: Discussioncontrasting

confidence: 99%

Up-regulation of SOCS4 promotes cell proliferation and migration in esophageal squamous cell carcinoma

Ying¹,

Huang²,

Zhang³

et al. 2021

Transl Cancer Res TCR

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Background: Suppressors 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. Methods:The 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.Results: In 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.Conclusions: These 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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Section: Discussioncontrasting

confidence: 99%

Up-regulation of SOCS4 promotes cell proliferation and migration in esophageal squamous cell carcinoma

Ying¹,

Huang²,

Zhang³

et al. 2021

Transl Cancer Res TCR

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“…The activation of the TLR7/8 signaling pathway led to the activation of NF-κB which was required for the induction of TNF-α [17]. SOCS3, as a suppressor of cytokine signaling, has been implicated in transcriptional activation of signal transduction and activators of transcription (STAT) signaling pathway [18][19][20]. SOCS3 is up-regulated in response to various cytokines such as TNF-α, IL-6 and growth hormone [21].…”

Section: Discussionmentioning

confidence: 99%

Identification of novel biomarkers and candidate small molecule drugs in rheumatoid arthritis and osteoarthritis based on bioinformatics analysis of high-throughput data

et al. 2020

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Background: Rheumatoid arthritis (RA) and osteoarthritis (OA) are two major types of joint diseases. The present study aimed to identify hub genes involved in the pathogenesis and further explore the potential treatment targets of RA and OA. Methods: The gene expression profile of GSE12021 was downloaded from Gene Expression Omnibus (GEO). Total 31 samples (12 RA, 10 OA and 9 NC samples) were used. The differentially expressed genes (DEGs) in RA versus NC, OA versus NC and RA versus OA groups were screened using limma package. We also verified the DEGs in GSE55235 and GSE100786. Functional annotation and protein–protein interaction (PPI) network construction of OA- and RA-specific DEGs were performed. Finally, the candidate small molecules as potential drugs to treat RA and OA were predicted in CMap database. Results: 165 up-regulated and 163 down-regulated DEGs between RA and NC samples, 73 up-regulated and 293 down-regulated DEGs between OA and NC samples, 92 up-regulated and 98 down-regulated DEGs between RA and OA samples were identified. Immune response and TNF signaling pathway were significantly enriched pathways for RA- and OA-specific DEGs, respectively. The hub genes were mainly associated with ‘Primary immunodeficiency’ (RA vs. NC group), ‘Ribosome’ (OA vs. NC group), and ‘Chemokine signaling pathway’ (RA vs. OA group). Arecoline and Cefamandole were the most promising small molecule to reverse the RA and OA gene expression. Conclusion: Our findings suggest new insights into the underlying pathogenesis of RA and OA, which may improve the diagnosis and treatment of these intractable chronic diseases.

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“…CIS and SOCS1-3 implement a negative feedback loop of cytokine signaling, and other SOCSs primarily control growth factor receptor signaling [220]. Additionally, modulation of NF-κB activity by SOCS1 and SOCS3 has been documented [221]. Proteins of the SOCS family can mark their targets for degradation by the ubiquitin pathway and inhibit the activity of enzymes by competing with substrates.…”

Section: Jak-stat Signaling Componentsmentioning

confidence: 99%

Innate-Immunity Genes in Obesity

Михайлова

Ivanoshchuk

2021

JPM

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The main functions of adipose tissue are thought to be storage and mobilization of the body’s energy reserves, active and passive thermoregulation, participation in the spatial organization of internal organs, protection of the body from lipotoxicity, and ectopic lipid deposition. After the discovery of adipokines, the endocrine function was added to the above list, and after the identification of crosstalk between adipocytes and immune cells, an immune function was suggested. Nonetheless, it turned out that the mechanisms underlying mutual regulatory relations of adipocytes, preadipocytes, immune cells, and their microenvironment are complex and redundant at many levels. One possible way to elucidate the picture of adipose-tissue regulation is to determine genetic variants correlating with obesity. In this review, we examine various aspects of adipose-tissue involvement in innate immune responses as well as variants of immune-response genes associated with obesity.

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SOCS3 control the activity of NF-κB induced by HSP70viadegradation of MyD88-adapter-like protein (Mal) in IPEC-J2 cells

Cited by 16 publications

References 41 publications

Up-regulation of SOCS4 promotes cell proliferation and migration in esophageal squamous cell carcinoma

Up-regulation of SOCS4 promotes cell proliferation and migration in esophageal squamous cell carcinoma

Identification of novel biomarkers and candidate small molecule drugs in rheumatoid arthritis and osteoarthritis based on bioinformatics analysis of high-throughput data

Innate-Immunity Genes in Obesity

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