Establishment of a Screening System for Chemicals that Upregulate a Melanoma Antigen, Melan-A/MART-1

Song, Hai Zhen; Kono, Michihiro; Tomita, Yasushi

doi:10.1620/tjem.217.231

Cited by 3 publications

(2 citation statements)

References 20 publications

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“…To begin to test this, we sought to generate a fluorescent Mart-1:GFP reporter construct that, when introduced into cells, would provide a vital, dynamic readout of changes in Mart-1 expression. Using a Mart-1 reporter plasmid tested in melanoma cells (kind gift from Michihiro Konno, Nagoya University; Song et al, 2009 ), we generated a lentiviral Mart-1:GFP promoter reporter plasmid and stably infected both C8161 metastatic and C81-61 non-metastatic melanoma cell lines, co-labeled with nuclear localized H2B-mCherry ( Fig. 1 A).…”

Section: Resultsmentioning

confidence: 99%

NGF reprograms metastatic melanoma to a bipotent glial-melanocyte neural crest-like precursor

et al. 2017

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Melanoma pathogenesis from normal neural crest-derived melanocytes is often fatal due to aggressive cell invasion throughout the body. The identification of signals that reprogram de-differentiated, metastatic melanoma cells to a less aggressive and stable phenotype would provide a novel strategy to limit disease progression. In this study, we identify and test the function of developmental signals within the chick embryonic neural crest microenvironment to reprogram and sustain the transition of human metastatic melanoma to a neural crest cell-like phenotype. Results reveal that co-culture of the highly aggressive and metastatic human melanoma cell line C8161 upregulate a marker of melanosome formation (Mart-1) in the presence of embryonic day 3.5 chick trunk dorsal root ganglia. We identify nerve growth factor (NGF) as the signal within this tissue driving Mart-1 re-expression and show that NGF receptors trkA and p75 cooperate to induce Mart-1 re-expression. Furthermore, Mart-1 expressing C8161 cells acquire a gene signature of poorly aggressive C81-61 cells. These data suggest that targeting NGF signaling may yield a novel strategy to reprogram metastatic melanoma toward a benign cell type.

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Section: Resultsmentioning

confidence: 99%

NGF reprograms metastatic melanoma to a bipotent glial-melanocyte neural crest-like precursor

et al. 2017

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“…The protein Melan-A (MLANA), also known as melanoma antigen recognized by T cells 1 or MART-1, is a protein that in humans is encoded by the MLANA or "MALENA" gene. A fragment of the protein, usually consisting of the 9 amino acids from 27 to 35, is bound by major histocompatibility complex Class I complexes, which present the fragment to T cells of the immune system (Baren, Baurain, Brasseur, & Coulie, 2012;Song, Kono, & Tomita, 2009). Melan-A, also known as MART-1 (melanoma antigen recognized by T cells-1), is one of the most important melanocytic markers.…”

Section: Discussionmentioning

confidence: 99%

Identification of pathogenic genes and transcription factors in vitiligo

Yuan

Meng

Cao

et al. 2019

Dermatologic Therapy

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Our study aimed to identify the key genes and upstream regulators in vitiligo. To screen the pathogenic genes of vitiligo, an integrated analysis was performed by using the microarray datasets in vitiligo derived from the Gene Expression Omnibus (GEO) database. The functional annotation and potential pathways of differentially expressed genes (DEGs) were further explored by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. We constructed a vitiligo‐specific transcriptional regulatory network to identify crucial transcriptional factors that target the DEGs in vitiligo. From two GEO datasets, we identified 1863 DEGs (744 downregulated DEGs and 1,119 upregulated DEGs [false discovery rate < 0.05, |Combined.ES| > 1]) between lesional tissues and nonlesional tissues. GO and KEGG analyses revealed that ubiquitin‐mediated proteolysis and the endoplasmic reticulum were significantly enriched pathways for DEGs. The expressions of premelanosome (PMEL), melan‐A (MLANA), dopachrome tautomerase (DCT), SRY‐boxtranscription factor 10 (SOX10), tyrosinase‐related protein 1 (TYRP1), and melanocortin 1 receptor (MC1R) were shown to be involved in the pathogenesis of vitiligo. We concluded that PMEL, MLANA), DCT, SOX10, TYRP1, and MC1R may play a role in vitiligo, among which TYRP1 and MC1R are regulated by forkhead box J2 (FOXJ2). Our finding may contribute to the development of new potential biomarkers, reveal the underlying pathogenesis of vitiligo, and identify novel therapeutic targets for vitiligo.

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Levosulpiride-loaded nanostructured lipid carriers for brain delivery with antipsychotic and antidepressant effects

et al. 2022

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Establishment of a Screening System for Chemicals that Upregulate a Melanoma Antigen, Melan-A/MART-1

Cited by 3 publications

References 20 publications

NGF reprograms metastatic melanoma to a bipotent glial-melanocyte neural crest-like precursor

NGF reprograms metastatic melanoma to a bipotent glial-melanocyte neural crest-like precursor

Identification of pathogenic genes and transcription factors in vitiligo

Levosulpiride-loaded nanostructured lipid carriers for brain delivery with antipsychotic and antidepressant effects

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