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Melanoma is the most aggressive type of skin cancer, exhibiting extensive local invasion and early distant metastasis. Aberrant expression of ubiquitin-protein ligase E3C (UBE3C) plays a key role in tumor development and progression. In the present study, we analyzed UBE3C expression in samples of cancerous and normal skin tissue. Levels of UBE3C expression were much higher in primary and metastatic melanoma tissues than in normal skin, cutaneous squamous cell carcinoma or basal cell carcinoma. Melanoma cells overexpressing UBE3C frequently exhibited a mesenchymal phenotype, including reduced expression of the epithelial marker E-cadherin and expression of the mesenchymal marker vimentin. Knockdown of UBE3C expression in melanoma cells significantly suppressed melanoma growth and progression. Furthermore, silencing UBE3C led to increased E-cadherin expression and decreased vimentin and Snail1 expression. Thus UBE3C promotes melanoma progression, possibly by inducing epithelial-mesenchymal transition in melanoma cells. Inhibiting UBE3C activity may suppress melanoma invasion and metastasis and may represent a targeted therapeutic approach.

Background: To investigate the role of DTL in the development of skin cutaneous melanoma (SKCM) and possible mechanisms. Methods:We examined the expression of DTL in SKCM in The Cancer Genome Atlas (TCGA) and Oncomine database and analyzed the relationship between DTL expression and melanoma prognosis.Furthermore, we silenced the DTL gene by RNA interference in A375 cells and investigated the effect of DTL silencing on the biological function of melanoma cells. Results:The expression of DTL in SKCM was upregulated in the tumor tissues compared with the paired normal tissues. Survival analysis showed that higher DTL expression in SKCM patients was associated with poor clinical outcome compared with the lower DTL expression group. Silencing of DTL in A375 cells significantly inhibited the melanoma cell growth and proliferation ability, and also significantly decreased the total glucose consumption and lactate production. Gene set enrichment analysis (GSEA) showed that MYC targets gene set pathway was highly enriched in the DTL high expression group. The expression levels of some MYC targets-related oncogenes, including c-MYC,

The association of psoriasis with thyroid dysfunction has been investigated. However, it remains unclear; some papers indicate it, and others do not. In this study, we evaluate the prevalence of thyroid dysfunction in patients with psoriasis vulgaris (PsV), psoriatic arthritis (PsA), generalized pustular psoriasis (GPP) and erythrodermic psoriasis (EP), and the association of thyroid dysfunction with inflammation. Data on 201 psoriatic patients visiting our hospital from January 2014 to November 2017 (159 men and 42 women; 74 PsV, 42 PsA, 38 GPP and 47 EP) were retrospectively analyzed. Thirty‐three percent of psoriatic patients had thyroid dysfunction. The percentage of patients with thyroid dysfunction was the highest in those with EP (60% EP, 42% GPP, 19% PsA, 19% PsV). The prevalence of thyroid dysfunction decreased significantly when patients switched from EP to PsV or PsA (58% vs 17%; median, 20.5; range, 4–65 months). Most of the patients with thyroid dysfunction had low thyroxine syndrome (serum levels of free thyroxine are low, but serum thyroid‐stimulating hormone level is normal). Patients with thyroid dysfunction demonstrated significantly higher CD3+ and CD4+ T‐cell absolute count levels than those without thyroid dysfunction. Meanwhile, patients with thyroid dysfunction demonstrated lower immunoglobulin (Ig)A and IgM levels than those without thyroid dysfunction. Finally, patients with thyroid dysfunction demonstrated higher elevated serum C‐reactive protein levels than those without dysfunction in total, although there were no statistical differences. Our data indicate that thyroid dysfunction in patients with psoriasis may be associated with inflammation caused by psoriasis.