ALDH2 is a novel biomarker and exerts an inhibitory effect on melanoma.

Melanoma is a malignant skin tumor. This study aimed to explore and assess the effect of novel biomarkers on the progression of melanoma. Differently expressed genes (DEGs) were screened from GSE3189 and GSE46517 datasets of Gene Expression Omnibus database using GEO2R. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses were conducted based on the identified DEGs. Hub genes were identified and assessed using protein-protein interaction networks, principal component analysis, and receiver operating characteristic curves. Quantitative real-time polymerase chain reaction was employed to measure the mRNA expression levels. TIMER revealed the association between aldehyde dehydrogenase 2 (ALDH2) and tumor immune microenvironment. The viability, proliferation, migration, and invasion were detected by cell counting kit-8, 5-ethynyl-2'-deoxyuridine, wound healing, and transwell assays. Total 241 common DEGs were screened out from GSE3189 and GSE46517 datasets. We determined 6 hub genes with high prediction values for melanoma, which could distinguish tumor samples from normal samples. ALDH2, ADH1B, ALDH3A2, DPT, EPHX2, and GATM were down-regulated in A375 and SK-MEL-2 cells, compared with the human normal melanin cell line (PIG1 cells). ALDH2 was selected as the candidate gene in this research, presenting a high diagnostic and predictive value for melanoma. ALDH2 had a positive correlation with the infiltrating levels of immune cells in melanoma microenvironment. Overexpression of ALDH2 inhibited cell viability, proliferation, migration, and invasion of A375/SK-MEL-2 cells. ALDH2 is a new gene biomarker of melanoma, which exerts an inhibitory effect on melanoma.

Targetoid-like lesions and chilblain-like erythema manifested on hands and feet: A case of Rowell syndrome from China.

BACKGROUND: Rowell syndrome (RS) is an uncommon condition characterized by erythema multiforme (EM)-like lesions and lupus erythematosus. It is more common in females, and EM may be the first manifestation of the disease with positive autoantibodies, such as antinuclear antibody (ANA), SSA, SSB and rheumatoid factor. The pathogenesis of RS is unknown and is likely caused by drug induction, ultraviolet exposure and infection. METHOD: We describe a case of RS from China which presented as characteristic targetoid-like lesions and chilblain-like erythema on hands and feet. This is a case of RS in a female patient from the inpatient department of dermatology. RESULTS: A 41-year-old female with systemic lupus erythematosus exhibited chilblain-like erythema and characteristic EM lesions on her extremities. She tested positive for serum ANA (1:320) and anti-double-stranded DNA, as well as other autoantibodies. Systemic glucocorticoids and hydroxychloroquine worked effectively for her. CONCLUSION: The present case met diagnostic criteria of RS. Notably, there was a co-occurrence of facial butterfly erythema, chilblain-like erythema and EM lesions distributed on the limbs in this case.

A systematic review and meta-analysis on the efficacy and safety of traditional Chinese medicine bath in the treatment of psoriasis vulgaris.

BACKGROUND: To clarify the efficacy and safety of traditional Chinese medicine (TCM) bath in the treatment of psoriasis vulgaris, meta-analysis and systematic evaluation were adopted to comprehensively evaluate the published articles. METHODS: Combing the terms "traditional Chinese medicine bath" and "psoriasis vulgaris", the articles were searched for in the databases of China Knowledge Network (CNKI), Baidu scholar, Wanfang, Chinese Biomedical Literature Database (CBM), Weipu Database, Medline, Embase, Chinese Medical Citation Index (CMCI), and PubMed. The quality of articles was evaluated using the RevMan 5.3 software provided by the Cochrane system. RESULTS: A total of 13 articles were included. From the funnel chart drawn, it could be seen that the circles and the midline of most articles were not symmetrical, and the publication was biased, so the conclusions obtained were relatively credible. The heterogeneity analysis of TCM bath in treatment of psoriasis vulgaris showed that 13 articles reporting the total effective rate (TER) and the TERs of the two groups displayed obvious differences [P<0.05, 95% confidence interval (CI): 2.9 to 4.77]; there were 8 articles reporting the incidence of adverse reactions, and the incidence of adverse reactions between the two groups was greatly different (P<0.05, 95% CI: 0.22 to 0.77); and there were 9 articles reporting the psoriasis area and severity index, and the overall efficacy was greatly different between the two groups (P<0.05, 95% CI: -5.38 to -1.88). DISCUSSION: The TER of the meta-analysis of treatment in this study was higher in the experimental group; the incidence of adverse reactions was lower in the experimental group; and the area and severity of psoriasis were lower in the experimental group, so it was concluded that the TCM bath had a significant effect on the treatment of psoriasis vulgaris.

Neferine induces p38 MAPK/JNK1/2 activation to modulate melanoma proliferation, apoptosis, and oxidative stress.

BACKGROUND: Melanoma is a malignant skin cancer that has a poor prognosis in advanced patients. The aim of the present study was to investigate the antitumor role of neferine in melanoma. METHODS: A375 and C32 cells were selected as research vectors in vitro. Cell counting Kit-8, 5-ethynyl-2'-deoxyuridine staining, transwell, and flow cytometry assay were used to examined cell malignant phenotypes. Mitochondrial dysfunction was detected by 5,50,6,60-tetrachloro-1,10,3,30-tetraethyl-imidacarbocyanine iodide staining and enzyme-linked immunosorbent assay. Reactive oxygen species (ROS) generation was measured using oxidation sensitive fluorescent probe. The phosphorylation activity of p38 and Jun-N-terminal kinase (JNK) 1/2 were examined by Western blot. A xenograft model was established via the subcutaneous injection of A375 cells into the right flank of BALB/c mice in vivo. RESULTS: Neferine (2.5, 5, or 10 µM) treatment inhibited proliferation, invasion, and enhanced apoptotic rate of A375 and C32 cells. Neferine treatment induced abnormal changes in mitochondrial membrane potential. Further studies showed that neferine could significantly increase the production of reactive oxygen species (ROS) and 3,4-methylenedioxyamphetamine (MDA) content, decreased the superoxide dismutase (SOD) level. Neferine (5, 10, or 20 mg/kg) obviously suppressed the weight and size of the xenograft tumor, the number of apoptotic cells in vivo, and the expression of Ki67+ and survivin+ decreased. Notably, neferine also activated the phosphorylation of p38 and JNK1/2. CONCLUSIONS: Neferine inhibits the proliferative and invasion ability of melanoma cells and promotes their apoptosis, ameliorating the malignant progression of melanoma, likely achieved by upregulating the phosphorylation levels of p38 mitogen-activated protein kinase and JNK1/2.