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Transcription factor LSF (TFCP2) inhibits melanoma growth

Late SV40 factor 3 (LSF), a transcription factor, contributes to human hepatocellular carcinoma (HCC). However, decreased expression level of LSF in skin melanoma compared to that in benign melanocytic tumors and nevi in mice and humans was found in this study. Anchorage-dependent and -independent g...

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Detalles Bibliográficos
Autores principales: Goto, Yuji, Yajima, Ichiro, Kumasaka, Mayuko, Ohgami, Nobutaka, Tanaka, Asami, Tsuzuki, Toyonori, Inoue, Yuji, Fukushima, Satoshi, Ihn, Hironobu, Kyoya, Mikiko, Ohashi, Hiroyuki, Kawakami, Tamihiro, Bennett, Dorothy C., Kato, Masashi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4823042/
https://www.ncbi.nlm.nih.gov/pubmed/26506241
http://dx.doi.org/10.18632/oncotarget.6230
Descripción
Sumario:Late SV40 factor 3 (LSF), a transcription factor, contributes to human hepatocellular carcinoma (HCC). However, decreased expression level of LSF in skin melanoma compared to that in benign melanocytic tumors and nevi in mice and humans was found in this study. Anchorage-dependent and -independent growth of melanoma cells was suppressed by LSF overexpression through an increased percentage of G1 phase cells and an increased p21(CIP1) expression level in vitro and in vivo. Anchorage-dependent growth in LSF-overexpressed melanoma cells was promoted by depletion of LSF in the LSF-overexpressed cells. Integrated results of our EMSA and chromatin immunoprecipitation assays showed binding of LSF within a 150-bp upstream region of the transcription start site of p21CIP1 in melanoma cells. Taken together, our results suggest potential roles of LSF as a growth regulator through control of the transcription of p21(CIP1) in melanocytes and melanoma cells as well as a biomarker for nevus.