Transcription factor LSF (TFCP2) inhibits melanoma growth

Yuji Goto, Ichiro Yajima, Mayuko Kumasaka, Nobutaka Ohgami, Asami Tanaka, Toyonori Tsuzuki, Yuji Inoue, Satoshi Fukushima, Hironobu Ihn, Mikiko Kyoya, Hiroyuki Ohashi, Tamihiro Kawakami, Dorothy C. Bennett, Masashi Kato

Research output: Contribution to journalArticlepeer-review

20 Citations (Scopus)


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 p21CIP1 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 p21CIP1 in melanocytes and melanoma cells as well as a biomarker for nevus.

Original languageEnglish
Pages (from-to)2379-2390
Number of pages12
Issue number3
Publication statusPublished - 2016
Externally publishedYes


  • CDKN1A
  • Cell cycle
  • Melanoma
  • TFCP2
  • Transcription factor LSF

ASJC Scopus subject areas

  • Oncology


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