Staphylococcal nuclease domain containing‐1 (SND1) promotes migration and invasion via angiotensin II type 1 receptor (AT1R) and TGFβ signaling

Santhekadur, Prasanna K.; Akiel, Maaged; Emdad, Luni; Gredler, Rachel; Srivastava, Jyoti; Rajasekaran, Devaraja; Robertson, Chadia L.; Mukhopadhyay, Nitai D.; Fisher, Paul B.; Sarkar, Devanand

doi:10.1016/j.fob.2014.03.012

Cited by 46 publications

(58 citation statements)

References 32 publications

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“…Other tumor-associated genes found to be mutated as single events in individual tumors in the SCOs within our cohort include FAT atypical cadherin 1 ( FAT1 ) [15], staphylococcal nuclease domain-containing protein 1 ( SND1 ) [16, 17], Cbl proto-oncogene E3 ubiquitin protein ligase ( CBL ), frizzled class receptor 7 ( FZD7 ), phosphatidylinositol-4,5-bisphosphate 3-kinase subunit gamma ( PIK3CG ), and SH3 domain binding kinase 1 ( SBK1 ).…”

Section: Resultsmentioning

confidence: 99%

“…Case 2 contained a mutation in SND1 , which has been reported to be involved in glioblastoma and carcinomas of the colon, prostate, and liver [16, 18–20]. SND1 is a component of the RNA-induced silencing complex (RISC) and has been reported to activate the MAP kinase ERK [17]. Case 1 contained a mutation in the tumor suppressor FAT1 atypical cadherin gene, which has been implicated in glioblastoma, colorectal adenocarcinoma, and head and neck squamous cell carcinoma [15].…”

Section: Discussionmentioning

confidence: 99%

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MAPK activation andHRASmutation identified in pituitary spindle cell oncocytoma

Miller

Ramkissoon

et al. 2016

Oncotarget

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Pituitary spindle cell oncocytoma (SCO) is an uncommon primary pituitary neoplasm that presents with mass effect on adjacent neurovascular structures, similar to non-hormone-producing pituitary adenomas. To determine the molecular etiology of SCO, we performed exome sequencing on four SCO cases, with matched normal controls, to assess somatic mutations and copy number alterations. Our analysis revealed a low mutation rate and a copy-neutral profile, consistent with the low-grade nature of this tumor. However, we identified a co-occurring somatic HRAS (p.Q61R) activating point mutation and MEN1 frameshift mutation (p.L117fs) present in a primary and recurrent tumor from one patient. Other SCOs demonstrated mutations in SND1 and FAT1, which are associated with MAPK pathway activation. Immunohistochemistry across the SCO cohort demonstrated robust MAPK activity in all cases (n=4), as evidenced by strong phospho-ERK staining, while phospho-AKT levels suggested only basal levels of PI3K pathway activation. Taken together, this identifies the MAPK signaling pathway as a novel therapeutic target for spindle cell oncocytoma, which may offer a powerful adjunct for aggressive tumors refractory to surgical resection.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

MAPK activation andHRASmutation identified in pituitary spindle cell oncocytoma

Miller

Ramkissoon

et al. 2016

Oncotarget

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“…Chronic inflammation is a critical event in HCC pathogenesis and induction by inflammatory cytokines might underlie the overexpression of SND1 in human HCC patients. Overexpression and knockdown studies in human HCC cells have demonstrated that SND1 promotes proliferation, migration, invasion and in vivo tumorigenesis [38][39][40][41] . As a component of the RISC in HCC cells, SND1 promotes oncogenic miRNA-mediated degradation of tumor suppressor mRNAs [38] [ Figure 2].…”

Section: Snd1 As An Oncogene For Hccmentioning

confidence: 99%

“…However, when overexpressed, SND1 could significantly augment RISC activity in human HCC cells when compared to normal hepatocytes [38] . By binding to and stabilizing angiotensin II type 1 receptor (AT1R) mRNA, SND1 activates TGFb and ERK signaling, thereby promoting epithelial-mesenchymal transition (EMT), in vitro migration and invasion by HCC cells [39] . In HCC cells, SND1 activates NF-κB, resulting in induction of miR-221 and angiogenic factors angiogenin and CXCL16 that promote tumor angiogenesis [40] .…”

Section: Snd1 As An Oncogene For Hccmentioning

confidence: 99%

The multifaceted oncogene SND1 in cancer: focus on hepatocellular carcinoma

Chidambaranathan-Reghupaty

Mendoza

Fisher

et al. 2018

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Staphylococcal nuclease and tudor domain containing 1 (SND1) is a protein that regulates a complex array of functions. It controls gene expression through transcriptional activation, mRNA degradation, mRNA stabilization, ubiquitination and alternative splicing. More than two decades of research has accumulated evidence of the role of SND1 as an oncogene in various cancers. It is a promoter of cancer hallmarks like proliferation, invasion, migration, angiogenesis and metastasis. In addition to these functions, it has a role in lipid metabolism, inflammation and stress response. The participation of SND1 in such varied functions makes it distinct from most oncogenes that are relatively more focused in their role. This becomes important in the case of hepatocellular carcinoma (HCC) since in addition to typical cancer drivers, factors like lipid metabolism deregulation and chronic inflammation can predispose hepatocytes to HCC. The objective of this review is to provide a summary of the current knowledge available on SND1, specifically in relation to HCC and to shed light on its prospect as a therapeutic target.

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“…This gene was first cloned by Yanaka et al, both in human and mouse [78, 79]. The expression of NPR-C is also ubiquitous and is known to be expressed in heart, lung, adrenal gland, heart, cerebral cortex, cerebellum, liver and adipocytes and in some cancers [80, 81]. The expression of NPR-C is influenced by various physiological factors and is reported to be very high in hypertensive, diabetic and obese patients [80].…”

Section: Natriuretic Peptide Receptorsmentioning

confidence: 99%

The multifaceted role of natriuretic peptides in metabolic syndrome

Santhekadur

Kumar

Seneshaw

et al. 2017

Biomedicine & Pharmacotherapy

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Due to globalization and sophisticated western and sedentary lifestyle, metabolic syndrome has emerged as a serious public health challenge. Obesity is significantly increasing worldwide because of increased high calorie food intake and decreased physical activity leading to hypertension, dyslipidemia, atherosclerosis, and insulin resistance. Thus, metabolic syndrome constitutes cardiovascular disease, type 2 diabetes, obesity, and nonalcoholic fatty liver disease (NAFLD) and recently some cancers are also considered to be associated with this syndrome. There is increasing evidence of the involvement of natriuretic peptides (NP) in the pathophysiology of metabolic diseases. The natriuretic peptides are cardiac hormones, which are produced in the cardiac atrium, ventricles of the heart and the endothelium. These peptides are involved in the homeostatic control of body water, sodium intake, potassium transport, lipolysis in adipocytes and regulates blood pressure. The three known natriuretic peptide hormones present in the natriuretic system are atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and c-type natriuretic peptide (CNP). These three peptides primarily function as endogenous ligands and mainly act via their membrane receptors such as natriuretic peptide receptor A (NPR-A), natriuretic peptide receptor B (NPR-B) and natriuretic peptide receptor C (NPR-C) and regulate various physiological and metabolic functions. This review will shed light on the structure and function of natriuretic peptides and their receptors and their role in the metabolic syndrome.

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Staphylococcal nuclease domain containing‐1 (SND1) promotes migration and invasion via angiotensin II type 1 receptor (AT1R) and TGFβ signaling

Cited by 46 publications

References 32 publications

MAPK activation andHRASmutation identified in pituitary spindle cell oncocytoma

MAPK activation andHRASmutation identified in pituitary spindle cell oncocytoma

The multifaceted oncogene SND1 in cancer: focus on hepatocellular carcinoma

The multifaceted role of natriuretic peptides in metabolic syndrome

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