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Together, our data provide important evidence for miR-19 mediated SOCS6 in OS growth and revealed miR-19/SOCS6/JAK2/STAT3 pathway as a potential therapeutic strategy for OS patients.
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Results indicate that similar to PTEN pseudogene (PTENP1), suppressor of cytokine signaling 6 protein (SOCS6) expression was also significantly lower in esophageal squamous cell carcinoma (ESCC) samples.
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our results describe for the first time the role of miR-494-3p during normal hematopoietic stem/progenitor cells differentiation and suggest that its increased expression, and the subsequent downregulation of its target SOCS6, might contribute to the megakaryocyte hyperplasia commonly observed in primary myelofibrosis patients.
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miR-142-3p regulates NPC development by down-regulating SOCS6 expression and suggest that modulation of miR-142-3p expression could be a therapeutic strategy for NPC
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Stage-independent downregulation of SOCS2 and SOCS6 correlate with disease-free survival in colorectal cancer.
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Studied both the function of upregulated miR-424-5p in pancreatic cancer and how downstream suppressor of cytokine-induced signaling 6 (SOCS6) is negatively regulated by miR-424-5p.
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miR-17-5p might function as a pro-proliferative factor by repressing SOCS6 in gastric cancer
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SOCS2 and SOCS6 expression are remarkably reduced in hepatocellular carcinoma and correlate with aggressive tumor progression and poor prognosis
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Results show that SOCS6 forms complex with DRP1 and the mitochondrial phosphatase PGAM5, attenuates DRP1 phosphorylation, and promotes DRP1 mitochondrial translocation.
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SOCS6 negatively regulates Flt3 activation, the downstream Erk signaling pathway, and cell proliferation.
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Reduced copy number and mRNA expression of SOCS6 are associated with disease recurrence in primary lung squamous cell carcinoma and may be useful prognostic biomarkers.
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The results may contribute to understanding SOCS5 and SOCS6 expression regulation in various cancer tissues, and show that these two factors may be used for diagnosing cancer.
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SOCS6 has ubiquitin ligase activity toward c-KIT
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These results establish that SOCS-6 acts as a negative regulator of T cell activation by promoting ubiquitin-dependent proteolysis of p56(lck).
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Data support the importance of loss-of-function of SOCS6 as a frequent event in gastric tumorigenesis.
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HOIL-1 expression stabilizes SOCS6 and induces the ubiquitination and degradation of proteins associated with SOCS6
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These observations suggest that Erk activation may be correlated in the cells with high expression of SOCS6.
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These observations suggest that SOCS6 is composed of at least two functional domains required for its biological role in localizing and degrading Stat3 in the nucleus.
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Study demonstrated that hypermethylation of the SOCS6 promoter is one of the mechanisms for the epigenetic regulation of SOCS6 expression.
