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MITF functions as a tumor suppressor in non-small cell lung cancer beyond the canonically oncogenic role

Yi-Jing Hsiao1, Wen-Hsin Chang2, Hsuan-Yu Chen3

  • 1Department of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, Taipei, Taiwan.

Aging
|December 9, 2020
PubMed

Insights

Microphthalamia-associated transcription factor (MITF) acts as a tumor suppressor in non-small cell lung cancer (NSCLC). Lower MITF expression correlates with poorer survival, while its silencing promotes tumor progression and metastasis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Microphthalamia-associated transcription factor (MITF) is crucial for melanocyte differentiation and is oncogenic in melanoma.
  • The function of MITF in non-small cell lung cancer (NSCLC) remains largely unexplored.

Purpose of the Study:

  • To investigate the role of MITF in the progression of non-small cell lung cancer (NSCLC).
  • To determine MITF's prognostic value and regulatory mechanisms in lung adenocarcinoma.

Main Methods:

  • Analysis of MITF expression in NSCLC tissues and cell lines.
  • In vitro and in vivo functional assays (cell migration, invasion, colony formation, xenograft models).
  • Whole transcriptome profiling and chromatin immunoprecipitation assays.

Main Results:

  • MITF is expressed in low-invasive lung adenocarcinoma and associated with better patient survival, acting as an independent prognostic marker.
  • MITF silencing enhances tumor cell migration, invasion, and metastasis, while decreasing angiogenesis.
  • MITF regulates cell development, cell cycle, inflammation, and WNT signaling, targeting genes like FZD7, PTGR1, and ANXA1.

Conclusions:

  • MITF exhibits a tumor-suppressive role in NSCLC, contrasting with its oncogenic function in melanoma.
  • MITF's suppressive effect is partly mediated through the regulation of downstream genes such as FZD7.
Keywords:
FZD7WNT pathwaymetastasistranscriptome profiling

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