SOCS6 is a selective suppressor of receptor tyrosine kinase signaling

Kabir, Nuzhat N.; Sun, Jianmin; Rönnstrand, Lars

doi:10.1007/s13277-014-2542-4

Cited by 34 publications

(32 citation statements)

References 58 publications

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“…Signaling downstream of FLT3 is tightly controlled by various signaling proteins which associate with FLT3 and regulate downstream signaling by propagating the signals from extracellular stimuli or diminish the signal by destabilizing the receptor. For example, association of GRB10, SLAP, SYK and CSK resulted in enhanced FLT3 signaling, while the association of SOCS6, SOCS2 and LNK suppressed FLT3 signaling by destabilizing the receptor [85][86][87][88][89][90][91][92][93][94][95]. BEX1 expression was found to be down-regulated in a group of FLT3-ITD positive AML patients [8].…”

Section: Bex Proteins In Acute Myeloid Leukemia (Aml)mentioning

confidence: 97%

Brain-Expressed X-linked (BEX) proteins in human cancers

Kazi

Kabir

2015

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

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The Brain-Expressed X-linked (BEX) family proteins are comprised of five human proteins including BEX1, BEX2, BEX3, BEX4 and BEX5. BEX family proteins are expressed in a wide range of tissues and are known to play a role in neuronal development. Recent studies suggest a role of BEX family proteins in cancers. BEX1 expression is lost in a subgroup of patients with acute myeloid leukemia (AML) and chronic myeloid leukemia (CML). Expression of BEX1 controls cell surface receptor signaling and restores imatinib response in resistant cells. BEX2 is overexpressed in a group of breast cancer patients and also in gliomas. Increased BEX2 expression led to enhanced NF-κB signaling as well as cell proliferation. Although BEX2 acts as tumor promoter in a subset of breast cancer, BEX3 expression displayed an opposite role. Overexpression of BEX3 resulted in inhibition of tumor formation in breast cancer mouse xenograft models. The role of BEX4 and BEX5 in cancer has not yet been defined. Collectively this suggests that BEX family members have distinct roles in cancers.While BEX1 and BEX3 act as a tumor suppressors, BEX2 seems to act as an oncogene.

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Section: Bex Proteins In Acute Myeloid Leukemia (Aml)mentioning

confidence: 97%

Brain-Expressed X-linked (BEX) proteins in human cancers

Kazi

Kabir

2015

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

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“…SOCS6 is a member of the SOCS family and participates in negative feedback regulation of receptor tyrosine kinase signaling [26,27]. Recently, SOCS6 was found to play essential roles in tumor development and tumorigenesis in various cancers.…”

Section: Cellular Physiology and Biochemistrymentioning

confidence: 99%

MiR-142-3p Suppresses SOCS6 Expression and Promotes Cell Proliferation in Nasopharyngeal Carcinoma

Zhou

et al. 2015

Cell Physiol Biochem

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Background/Aims: An increasing number of studies show that microRNAs (miRNAs) play crucial roles in nasopharyngeal carcinoma (NPC) tumorigenesis. The aim of our study was to investigate the biological roles and mechanisms of miR-142-3p in NPC. Methods: miR-142-3p expression was examined in NPC specimens and nasopharyngitis biopsy samples by quantitative real-time PCR. The biological functions of miR-142-3p were studied using a series of in vitro and in vivo approaches. Results: miR-142-3p is over-expressed in NPC tissues and cell lines. Knockdown of miR-142-3p significantly inhibited cell proliferation and cell cycle progression in vitro, and suppressed tumor growth in a mouse model. Suppressor of cytokine signaling 6 (SOCS6) was identified as a direct target of miR-142-3p, and miR-142-3p down-regulated the expression of SOCS6 by directly binding to its 3′untranslated region (UTR). Knockdown of SOCS6 abrogated the effects of miR-142-3p down-regulation. Conclusion: These findings indicate that miR-142-3p regulates NPC development by downregulating SOCS6 expression and suggest that modulation of miR-142-3p expression could be a therapeutic strategy for NPC.

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“…Suppressor of cytokine signaling 6 (SOCS6) is widely expressed in numerous tissues and is down-regulated in many cancers, including lung, colorectal, gastric, ovarian, stomach, thyroid, hepatocellular, and pancreatic cancer [5]. Reduced copy numbers and mRNA levels of SOCS6 are associated with disease recurrence in primary lung cancer, and thus may serve as useful prognostic biomarkers [6].…”

Section: Introductionmentioning

confidence: 99%

MiR-21 and MiR-155 promote non-small cell lung cancer progression by downregulating SOCS1, SOCS6, and PTEN

et al. 2016

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Lung cancer remains the leading cause of cancer-associated death worldwide. MiR-21 and miR-155 are the most amplified miRNAs in non-small cell lung carcinoma (NSCLC), and are critical promoters of NSCLC progression. However, it remains unclear how miR-21 and miR-155 induce cancer progression, and whether these miRNAs share common targets, such as tumor suppressor genes required to prevent NSCLC. Here we report that miR-21 and miR-155 levels are elevated in NSCLC and are proportional to the progression of the disease. In addition, miR-21 and miR-155 share nearly 30% of their predicted target genes, including SOCS1, SOCS6, and PTEN, three tumor suppressor genes often silenced in NSCLC. Consequently, antagonizing miR-21, miR-155 or both potently inhibited tumor progression in xenografted animal models of NSCLC. Treatment with miR-21 and miR-155 inhibitors in combination was always more effective against NSCLC than treatment with a single inhibitor. Furthermore, levels of miR-21 and miR-155 expression correlated inversely with overall and disease-free survival of NSCLC patients. Our findings reveal that miR-21 and miR-155 promote the development of NSCLC, in part by downregulating SOCS1, SOCS6, and PTEN. Combined inhibition of miR-21 and miR-155 could improve the treatment of NSCLC.

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SOCS6 is a selective suppressor of receptor tyrosine kinase signaling

Cited by 34 publications

References 58 publications

Brain-Expressed X-linked (BEX) proteins in human cancers

Brain-Expressed X-linked (BEX) proteins in human cancers

MiR-142-3p Suppresses SOCS6 Expression and Promotes Cell Proliferation in Nasopharyngeal Carcinoma

MiR-21 and MiR-155 promote non-small cell lung cancer progression by downregulating SOCS1, SOCS6, and PTEN

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