Suppressor of cytokine signaling (SOCS) genes are downregulated in breast cancer

Ghafouri‐Fard, Soudeh; Oskooei, Vahid Kholghi; Azari, Iman; Taheri, Mohammad

doi:10.1186/s12957-018-1529-9

Cited by 44 publications

(29 citation statements)

References 21 publications

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“…188 SOCS3 is downregulated in BC. 192 FXR may also mediate tumor effects through destabilization of hypoxia-inducible factor-1 alpha (HIF1-α), a master regulator that reprograms cancer cell metabolism and increases growth factors. [193][194][195] In addition, secondary BAs such as LCA also appear to be cytostatic through TGR5dependent effects on cancer cell metabolism, lipogenesis, epithelial mesenchymal transition (EMT), pro-and anti-apoptotic signaling, and anti-tumor immunity in vitro and in vivo.…”

Section: Can Bas Also Influence Bc? the Presence Of Bas In Breast Tissuementioning

confidence: 99%

Microbiome, bile acids, and obesity: How microbially modified metabolites shape anti‐tumor immunity

Sipe

Chaib

Pingili

et al. 2020

Immunological Reviews

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Bile acids (BAs) are known facilitators of nutrient absorption but recent paradigm shifts now recognize BAs as signaling molecules regulating both innate and adaptive immunity. Bile acids are synthesized from cholesterol in the liver with subsequent microbial modification and fermentation adding complexity to pool composition. Bile acids act on several receptors such as Farnesoid X Receptor and the G proteincoupled BA receptor 1 (TGR5). Interestingly, BA receptors (BARs) are expressed on immune cells and activation either by BAs or BAR agonists modulates innate and adaptive immune cell populations skewing their polarization toward a more tolerogenic anti-inflammatory phenotype. Intriguingly, recent evidence also suggests that BAs promote anti-tumor immune response through activation and recruitment of tumoricidal immune cells such as natural killer T cells. These exciting findings have redefined BA signaling in health and disease wherein they may suppress inflammation on the one hand, yet promote anti-tumor immunity on the other hand. In this review, we provide our readers with the most recent understanding of the interaction of BAs with the host microbiome, their effect on innate and adaptive immunity in health and disease with a special focus on obesity, bariatric surgery-induced weight loss, and immune checkpoint blockade in cancer. K E Y W O R D S bariatric surgery, immunometabolism, microbiome, mitochondria, obesity, tumor microenvironment | 221 SIPE Et al.

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Section: Can Bas Also Influence Bc? the Presence Of Bas In Breast Tissuementioning

confidence: 99%

Microbiome, bile acids, and obesity: How microbially modified metabolites shape anti‐tumor immunity

Sipe

Chaib

Pingili

et al. 2020

Immunological Reviews

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“…Signal transducer and activator of transcription 3 (STAT3) activation is counterbalanced by three main groups of negative regulators; phosphatases, Protein Inhibitor of Activated STAT (PIAS) proteins and Suppressor of Cytokine Signalling (SOCS) proteins [70][71][72][73][74]. While phosphatases up-regulated in cancer counteract the JAK-mediated phosphorylation or terminate the activation of STAT3 [70,71,75], PIAS proteins which are upregulated in breast cancer, inhibit STAT3 DNA binding activity [73,76], and SOCS proteins, that inhibit JAK-STAT3 signalling through negative feedback, are downregulated in breast cancer [77]. While the negative regulation actively modulates STAT3 activity, when compromised, it acts to synergistically enhance aberrant stimulation and constitutive activation of STAT3.…”

Section: Canonical Stat3 Signalling and The Warburg Effectmentioning

confidence: 99%

A STAT3 of Addiction: Adipose Tissue, Adipocytokine Signalling and STAT3 as Mediators of Metabolic Remodelling in the Tumour Microenvironment

Kadye

Stoffels

Fanucci

et al. 2020

Cells

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Metabolic remodelling of the tumour microenvironment is a major mechanism by which cancer cells survive and resist treatment. The pro-oncogenic inflammatory cascade released by adipose tissue promotes oncogenic transformation, proliferation, angiogenesis, metastasis and evasion of apoptosis. STAT3 has emerged as an important mediator of metabolic remodelling. As a downstream effector of adipocytokines and cytokines, its canonical and non-canonical activities affect mitochondrial functioning and cancer metabolism. In this review, we examine the central role played by the crosstalk between the transcriptional and mitochondrial roles of STAT3 to promote survival and further oncogenesis within the tumour microenvironment with a particular focus on adipose-breast cancer interactions.

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“…Suppressor of cytokine signalling (SOCS) proteins have been proven to be intracellular inhibitors of the JAK/STAT signalling pathway [25]. As reported, up-regulation of SOCS3 inhibited MMP-9 expression in retinal microglia induced by high glucose [26].…”

Section: Discussionmentioning

confidence: 94%

Regulation of the miR-19b-mediated SOCS6-JAK2/STAT3 pathway by lncRNA MEG3 is involved in high glucose-induced apoptosis in hRMECs

Xiao

Lan

et al. 2020

Bioscience Reports

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Objective: Diabetic retinopathy (DR) is one of the most severe and common complications of diabetes mellitus. The present study aimed to investigate the molecular mechanism of MEG3, miR-19b and SOCS6 in human retinal microvascular endothelial cells (hRMECs) under high glucose conditions. Methods: HRMECs were cultured in 5 or 30 mM D-glucose medium. qRT-PCR and Western blotting were used to determine the mRNA expression and protein levels. MTT assay and flow cytometry analysis were performed to detect the viability and apoptosis of hRMECs, respectively. TNF-α, IL-6 and IL-1β levels in cell supernatants were detected by ELISA. The activity of caspase-3/7 was also determined. A luciferase reporter assay was performed to confirm the targeting relationship between miR-19b and SOCS6, as well as MEG3 and miR-19b. Results: Our study demonstrated that miR-19b was increased and SOCS6 was decreased in HG-induced hRMECs. Knockdown of SOCS6 inhibited cell viability and reversed the promotion of cell viability induced by knockdown of miR-19b. Additionally, miR-19b directly targeted and negatively regulated SOCS6. Moreover, miR-19b promoted the cell apoptosis rate and caspase-3/7 activity and increased inflammatory factors through the SOCS6-mediated JAK2/STAT3 signalling pathway. In addition, MEG3 attenuated HG-induced apoptosis of hRMECs by targeting the miR-19b/SOCS6 axis. Conclusion: These findings indicate that MEG3 inhibited HG-induced apoptosis and inflammation by regulating the miR-19b/SOCS6 axis through the JAK2/STAT3 signalling pathway in hRMECs. Thus, these findings might provide a new target for the treatment of DR.

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Suppressor of cytokine signaling (SOCS) genes are downregulated in breast cancer

Cited by 44 publications

References 21 publications

Microbiome, bile acids, and obesity: How microbially modified metabolites shape anti‐tumor immunity

Microbiome, bile acids, and obesity: How microbially modified metabolites shape anti‐tumor immunity

A STAT3 of Addiction: Adipose Tissue, Adipocytokine Signalling and STAT3 as Mediators of Metabolic Remodelling in the Tumour Microenvironment

Regulation of the miR-19b-mediated SOCS6-JAK2/STAT3 pathway by lncRNA MEG3 is involved in high glucose-induced apoptosis in hRMECs

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