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To investigate whether PSGL-1 is correlated with the prognosis of cutaneous malignant melanoma. Genetic data of PSGL-1 and cutaneous malignant melanoma were extracted from genomewide association studies (GWAS) and analyzed using inverse variance weighting, MR-Egger regression, weighted median, weighted mode, and simple mode methods, and sensitivity analyses were performed on the data. Survival information of cutaneous malignant melanoma was extracted from the TCGA database, and grouped according to high and low PSGL-1 expression, survival curves were plotted by the Kaplan-Meier method, and the Log-rank test was used to compare the difference between the two survival periods. Exploring the effects of PSGL-1 on the biological functions of A375 cells through in vitro experiments. The inverse variance weighted method analysis of PSGL-1 on cutaneous malignant melanoma resulted in OR=0.666, 95% CI (0.494-0.899), P=0.008. The median survival was 44.70 months in the PSGL-1 high expression group and 29.13 months in the PSGL-1 low expression group, P=0.000 2. PSGL-1 inhibits the migration of A375 cells in vitro. Increased PSGL-1 expression is a protective factor against cutaneous malignant melanoma and is a potential prognostic marker for cutaneous melanoma. [ABSTRACT FROM AUTHOR]

Objective To explore the role of AlkB homologue 5 (ALKBH5) mediated m6A methylation modifications in the chemoradiotherapy resistance of cutaneous malignant melanoma (CMM). Methods From May 2019 to January 2021, the expression of ALKBH5 and NFE2L1 (nuclear factor, erythroid 2 like 1) in CMM cells was detected by real-time polymerase chain reaction (RT-PCR). TCGA was used to analyze the expression and correlation of ALKBH5 and NFE2L1. ALKBH5 was knocked down in CMM cells and the changes in m6A methylation expression of NFE2L1 was detected by immunoprecipitation. The role of ALKBH5 and NFE2L1 in chemoradiotherapy resistance of CMM cells was detected by MTT. Results The expression of both ALKBH5 and NFE2L1 in CMM cells was significantly higher than that in normal human epidermal melanocytes (P<0.05). The m6A methylation level of NFE2L1 mRNA was regulated by ALKBH5. In CMM cells with ALKBH5 knocked down, the survival rate of cells decreased and the chemoradiotherapy resistance reduced after irradiation and cisplatin treatment (P<0.05). After overexpression of NFE2L1, the survival rate of cells increased after treatment and the chemoradiotherapy resistance of CMM was induced (P<0.05). Conclusion ALKBH5 promoted chemoradiotherapy resistance of CMM by removing the m6A methylation modification of NFE2L1 and upregulating NFE2L1 expression. The effect of ALKBH5 on malignant phenotype of CMM was mediated through NFE2L1. [ABSTRACT FROM AUTHOR]

Objective To explore the effect of obesity-associated protein (FTO) and human homeobox protein 13(HOXB13) in cutaneous malignant melanoma (CMM) invasion and proliferation. Methods From January 2019 to December 2020, the expression of FTO and HOXB13 in CMM cells was detected by real-time polymerase chain reaction (RT-PCR). The expression and correlation of FTO and HOXB13 was analyzed by TCGA. The changes in expressionof n6-methyladenosine (m6A) of HOXB13 were detected by immunoprecipitation. The biological effects of FTO and HOXB13 on CMM cells proliferation and invasion was analyzed by CCK-8 and Transwell. Results Compared with normal cutaneous malignant melanoma, the expression level of FTO and HOXB13 in CMM cells was significantly increased (P<0.05). The methylation level of m6A of HOXB13 was regulated by FTO. After knocking down FTO in CMM cells, the proliferation and invasion ability was significantly reduced (P<0.05). After overexpression of HOXB13, the proliferation and invasion ability was significantly restored (P<0.05). The effect of FTO on malignant phenotype of CMM was achieved through HOXB13. Conclusion FTO can promote the proliferation and invasion of CMM cells by removing methylation modification of m6A of HOXB13 and up-regulating the expression of HOXB13. [ABSTRACT FROM AUTHOR]

Acral melanoma (AM) is the most common histologic subtype of melanoma in dark-skinned patients and is associated with a worse prognosis and a high mortality rate, largely due to the inconspicuous nature of early-stage lesions, which can lead to late diagnosis. Because of the overlapping clinical and histopathological features of AM with other forms of cutaneous melanomas, early detection of AM requires a multidisciplinary approach that integrates various diagnostic modalities, including clinical examination, dermoscopy, histopathology, molecular testing, radiological imaging, and blood tests. While surgery is the preferred method of treatment for AM, other therapeutic options may be employed based on the stage and underlying etiology of the disease. Immune checkpoint inhibitors, molecular targeted therapy, radiotherapy, chemotherapy, and oncolytic virotherapy represent promising advanced treatment options for AM. In this review, we provide an overview of the latest advancements in diagnostic and therapeutic methods for AM, highlighting the importance of early detection and the prompt, individualized management of this challenging disease.

Objective To observe the expression of sFRP-2 in cutaneous malignant melanoma cell lines and tissues and the effect of sFRP-2 on proliferation of cutaneous malignant melanoma cell lines A375 and to explore the mechanism. Methods The expression of sFRP-2 in cutaneous malignant melanoma cell lines and tissues and pathological characteristics were analyzed through qRT-PCR and immunohistochemistry. The A375 cells with lowest expression of sFRP-2 were selected as the experimental subjects. The lentivirus vectors pLVX-Gfp-sFRP-2 (experimental group) and pLVX-Gfp-NC (control group) was transfected into A375 cells, over-expression of sFRP-2 was detected by western blot. The effect of sFRP-2 on cell proliferation was analyzed by cell proliferation and colony formation assay. The effect of sFRP-2 on WNT/茁-catenin signaling pathway was confirmed by western blot. Results Compared with normal pigmented nevus, the expression of sFRP-2 mRNA and protein was downregulated in malignant melanoma cell lines and tissues(P<0.001). After over-expression of sFRP-2, the viability and proliferation of cells was significantly inhibited (P<0.001); WNT/β-catenin signaling pathway and its downstream cytokines were also significantly inhibited. Conclusion The expression of sFRP-2 in human cutaneous malignant melanoma was downregulated, which involved in the prcogress of cutaneous malignant melanoma by antagonizing Wnt/茁-catenin signaling pathway. [ABSTRACT FROM AUTHOR]