SOCS1: phosphorylation, dimerization and tumor suppression

Lessard, Frédéric; Saint-Germain, Emmanuelle; Mignacca, Lian; Ferbeyre, Gerardo

doi:10.18632/oncoscience.495

Cited by 10 publications

(10 citation statements)

References 19 publications

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“…Based on its protein structure, SOCS has two main functions: first, SOCS1 regulates cell proliferation and apoptosis as a signal inhibitor; second, SOCS1 regulates cell growth by participating in ubiquitination and mediating the degradation of ubiquitination substrate [ 28 ]. With the C-terminal SOCS box motif, SOCS1 can function as a tumor suppressor by reducing oncoproteins via ubiquitination mechanism [ 29 ]. SOCS1 directly or indirectly regulates many cancer-related molecules or pathways, including cyclin D1, cyclin-dependent kinase 4 (CDK4), mitogen-activated protein kinase (MAPK)/p38, p53, programmed cell death receptor ligand 1 (PD-L1), STAT3, STAT1, STAT6, etc.…”

Section: Discussionmentioning

confidence: 99%

Long Non-Coding RNA NORAD Inhibits Breast Cancer Cell Proliferation and Metastasis by Regulating miR-155-5p/SOCS1 Axis

Liu

Zhou

et al. 2021

J Breast Cancer

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Purpose Non-coding RNA activated by DNA damage (NORAD) has been reported to be a cancer-related long non-coding RNA (lncRNA) implicated in the progression of several cancers; however, its role in breast cancer (BC) has not yet been clarified. Methods Quantitative real-time polymerase chain reaction was used to examine NORAD, microRNA (miR)-155-5p, and suppressor of cytokine signaling 1 (SOCS1) mRNA expression levels. Western blotting was used to analyze SOCS1 protein expression. The malignancy of BC cells was assessed using the cell counting kit-8 (CCK-8), BrdU, and Transwell assays. Bioinformatics analysis, RNA immunoprecipitation assay, and dual-luciferase reporter gene assays were used to verify the targeted relationship between NORAD and miR-155-5p. Additionally, the regulatory effects of NORAD and miR-155-5p on SOCS1 expression were determined by western blotting. Results NORAD expression was significantly reduced in BC cell lines and tissues, and its low expression was associated with poor tumor tissue differentiation. NORAD overexpression repressed BC cell proliferation, migration, and invasion, whereas its knockdown produced the opposite effects. Additionally, miR-155-5p was found to be a target of NORAD, and the biological functions of miR-155-5p and NORAD were counteractive. MiR-155-5p was confirmed to target SOCS1, and SOCS1 was found to be positively regulated by NORAD. Conclusion NORAD suppresses miR-155-5p to upregulate SOCS1, thereby repressing the proliferation, migration, and invasion of BC cells.

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Section: Discussionmentioning

confidence: 99%

Long Non-Coding RNA NORAD Inhibits Breast Cancer Cell Proliferation and Metastasis by Regulating miR-155-5p/SOCS1 Axis

Liu

Zhou

et al. 2021

J Breast Cancer

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“…5 A and Table S2 ). SOCS1 can directly interact with P53, which leads to activation of its transcriptional program and induction of cellular apoptosis, ferroptosis and senescence 35 . Western blot analysis confirmed that treatment of 18097 increased protein expression of SOCS1 and P53 in cancer cells ( Fig.…”

Section: Resultsmentioning

confidence: 99%

A novel inhibitor of N6-methyladenosine demethylase FTO induces mRNA methylation and shows anti-cancer activities

Xie

Ling

et al. 2022

Acta Pharmaceutica Sinica B

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“…Treg participates in the immune response and maintains homeostasis together with Th17, mainly by secreting anti-in ammatory factors such as IL-10 to suppress in ammatory responses and maintain immune tolerance(38). SOCS1 can inhibit DCs maturation by suppressing JAK-STAT signaling pathway in DCs cells to maintain DCs stably in the imDCs state (39). It was found that SOCS1 could inhibit the conversion of Treg cells into Th17 cells (5).…”

Section: Discussionmentioning

confidence: 99%

Effects of Overexpressed SOCS1 Transfected DCs on Th17- and Treg-Related Cytokines in Mice with COPD

Liao¹,

Chen²,

Zhang³

et al. 2022

Preprint

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Background: In this study, we established a chronic obstructive pulmonary disease (COPD) model by stimulating mice with cigarette smoke, and observed the effects of dendritic cells (DCs) overexpressing SOCS1 on Th17, Treg and other related cytokines in peripheral blood, bronchoalveolar lavage fluid and lung tissues of COPD mice.Methods: After successfully transfecting DCs with overexpressing SOCS1 (DC-SOCS1), the mice were injected with DC-SOCS1 (1×106), DC-SOCS1 (2×106) and immature DCs (1×106) via tail vein on days 1 and 7 of COPD fumigation modeling. After day 28 of modeling, the peripheral blood, BALF and lung tissue samples were extracted from the mice, and the changes of DCs, Th17 and Treg cells and related cytokines were detected by immunohistochemistry, immunofluorescence, HE staining, flow cytometry and ELISA.Results: The results showed that DC-SOCS1 was able to reduce the secretion of pro-inflammatory factors and increase the anti-inflammatory factors in the COPD mice, and the effect of high concentration (2×106 DC-SOCS1) was better than low concentration (1×106 DC-SOCS1). Moreover, the intervention effect was significant on day 1 compared with day 7. In the mice injected with DC-SOCS1, the expression of CD83, IL-4, Foxp3, and CCR6 was increased on day 1 than those on day 7, while IL-17 and IFN-γ was decreased.Conclusions: Intervention of COPD mice with high concentrations of DCs-SOCS1 reduced pro-inflammatory factor secretion and attenuated the inflammatory response in COPD.Trial registration：Not applicable.

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SOCS1: phosphorylation, dimerization and tumor suppression

Cited by 10 publications

References 19 publications

Long Non-Coding RNA NORAD Inhibits Breast Cancer Cell Proliferation and Metastasis by Regulating miR-155-5p/SOCS1 Axis

Long Non-Coding RNA NORAD Inhibits Breast Cancer Cell Proliferation and Metastasis by Regulating miR-155-5p/SOCS1 Axis

A novel inhibitor of N6-methyladenosine demethylase FTO induces mRNA methylation and shows anti-cancer activities

Effects of Overexpressed SOCS1 Transfected DCs on Th17- and Treg-Related Cytokines in Mice with COPD

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