Effects of SASH1 on melanoma cell proliferation and apoptosis in vitro

Lin, Shiu‐Ru; Zhang, Junyu; Xu, Jie; Wang, Honglian; Sang, Qing; Xing, Qinghe; He, Lin

doi:10.3892/mmr.2012.1099

Cited by 27 publications

(32 citation statements)

References 28 publications

(34 reference statements)

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“…6,7 Consistent with the onset of carcinoma in the affected individuals in this study, SASH1 was recently reported to be involved in the tumorigenesis of several cancers. [15][16][17][18][19][20] Cellular experiments showed that SASH1 localizes to the nucleus and cytoplasm of epithelial cells and might regulate cellular migration and adhesion, through its role in protruding membrane structures. 21 Through its central SH3 domain, SASH1 interacts with the actin cytoskeleton and especially cortactin, a major regulator of actin filament dynamics.…”

Section: Discussionmentioning

confidence: 99%

“…SASH1 encodes a candidate tumor suppressor from the SLY family of signal proteins. [15][16][17][18][19][20] This variant was absent from Exome Variant Server, dbSNP and local exomes, predicted as deleterious by Condel and possibly damaging by Polyphen2, and comes from a well-conserved sequence (GERP conservation score: 5090) (see Web Resources). Cosegregation analysis in all available relatives confirmed its presence in a homozygous state in both affected patients (III.6 and III.3), in a heterozygous state in both parents and an unaffected brother (III7) and absent in the unaffected sister (III4).…”

Section: Genetic Investigationsmentioning

confidence: 99%

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Autosomal-recessive SASH1 variants associated with a new genodermatosis with pigmentation defects, palmoplantar keratoderma and skin carcinoma

et al. 2014

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9SASH1 (SAM and SH3 domain-containing protein 1) is a tumor suppressor gene involved in the tumorigenesis of a spectrum of solid cancers. Heterozygous SASH1 variants are known to cause autosomal-dominant dyschromatosis. Homozygosity mapping and whole-exome sequencing were performed in a consanguineous Moroccan family with two affected siblings presenting an unclassified phenotype associating an abnormal pigmentation pattern (hypo-and hyperpigmented macules of the trunk and face and areas of reticular hypo-and hyperpigmentation of the extremities), alopecia, palmoplantar keratoderma, ungueal dystrophy and recurrent spinocellular carcinoma. We identified a homozygous variant in SASH1 (c.1849G4A; p.Glu617Lys) in both affected individuals. Wound-healing assay showed that the patient's fibroblasts were better able than control fibroblasts to migrate. Following the identification of SASH1 heterozygous variants in dyschromatosis, we used reverse phenotyping to show that autosomal-recessive variants of this gene could be responsible for an overlapping but more complex phenotype that affected skin appendages. SASH1 should be added to the list of genes responsible for autosomal-dominant and -recessive genodermatosis, with no phenotype in heterozygous patients in the recessive form, and to the list of genes responsible for a predisposition to skin cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Genetic Investigationsmentioning

confidence: 99%

Autosomal-recessive SASH1 variants associated with a new genodermatosis with pigmentation defects, palmoplantar keratoderma and skin carcinoma

et al. 2014

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“…Recent studies from 2012 focusing on SASH1 function in cancer, 107,108,109,110 showed that SASH1 over-expression in different cancer cell lines lead to accumulation of cells in G0/G1 phase, indicating an inhibitory effect of SASH1 on cell proliferation. Accordingly, cyclin D1 levels were found lowered in all but one cell line and cell invasiveness in vitro assays showed that SASH1 overexpression lead to decreased invasiveness of the cancerous cells.…”

Section: Sash1 In Cancermentioning

confidence: 99%

SASH1, a new potential link between smoking and atherosclerosis

et al. 2015

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“…These results indicated that the down-regulation of SASH1 is at least in part due to gene deletion (13). Down-regulation of SASH1 expression was closely correlated with tumor invasion, metastasis, and poor prognosis (22)(23)(24). However, the specific role of SASH1 in ovarian carcinoma has not yet been reported in the literature.…”

Section: Introductionmentioning

confidence: 57%

“…SASH1 has been suggested as a candidate tumor suppressor. The reduction or absence SASH1 is closely related to tumor growth, invasion, metastasis, and poor prognosis (13,14,23,24). Zeller et al (13) reported that SASH1 mRNA expression was significantly reduced or completely absent in 6 breast cancer cell lines, and that it was also significantly decreased in primary thyroid cancers.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of SASH1 correlates with tumor progression and poor prognosis in ovarian carcinoma

et al. 2016

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Abstract. SAM-and SH3-domain containing 1 (SASH1) is a recently identified tumor suppressor gene that is required in the tumorigenesis of breast and other solid carcinomas. The SASH1 protein contains SH3 and SAM domains, indicating that it may serve an important role in intracellular signal transduction. The purpose of the present study was to investigate the expression of SASH1 in ovarian carcinoma and the correlation between its expression with clinical pathological features and clinical significance, and the effect of SASH1 on cell proliferation, apoptosis and migration of ovarian SKOV3 cells. The human ovarian carcinoma tissues and adjacent normal tissues were collected following surgery. Reverse transcription-quantitative polymerase chain reaction and western blot analysis were used to detect the expression levels of SASH1 mRNA and protein, respectively. The expression levels of SASH1 mRNA and protein in ovarian carcinoma tissues were significantly lower than that observed in adjacent normal tissues (P<0.05). The expression levels of SASH1 in samples from patients without lymph nodes metastasis and patients with early FIGO stage was lower than those with lymph nodes metastasis and patients with advanced FIGO stage (P<0.05). Flow cytometry analysis and Transwell invasion chamber experiments were used to investigate the effect of SASH1 on the cell proliferation, apoptosis and migration of SKOV3 cells. The recombinant plasmid pcDNA3.1-SASH1 was constructed and transfected into SKOV3 cells. In addition, the SKOV3 cells in the pcDNA3.1-SASH1 group exhibited significantly reduced cell growth, proliferation, and migration ability compared to the empty vector group and normal group (P<0.01). There were a greater number of apoptotic cells in the pcDNA3.1-SASH1 group compared to the empty vector group and normal group (P<0.01). Taken together, these results indicated that SASH1 may be a tumor suppressor gene in ovarian carcinoma, and SASH1 expression inhibited growth, proliferation and migration, and enhanced apoptosis of SKOV3 cells.

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Effects of SASH1 on melanoma cell proliferation and apoptosis in vitro

Cited by 27 publications

References 28 publications

Autosomal-recessive SASH1 variants associated with a new genodermatosis with pigmentation defects, palmoplantar keratoderma and skin carcinoma

Autosomal-recessive SASH1 variants associated with a new genodermatosis with pigmentation defects, palmoplantar keratoderma and skin carcinoma

SASH1, a new potential link between smoking and atherosclerosis

Downregulation of SASH1 correlates with tumor progression and poor prognosis in ovarian carcinoma

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