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The Janus-faced roles of Krüppel-like factor 4 in oral squamous cell carcinoma cells

Wenwen Li1, Man Liu1, Ying Su1

  • 1Beijing Institute of Dental Research, Stomatological Hospital and School of Stomatology, Capital Medical University, Beijing, China.

Oncotarget
|October 31, 2015
PubMed

Insights

Krüppel-like factor 4 (KLF4) expression is reduced in oral cancer due to promoter hypermethylation. KLF4 shows dual roles, suppressing tumors but promoting migration and invasion, suggesting complex involvement in oral cancer development.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Epigenetics

Background:

  • Krüppel-like factor 4 (KLF4) is a transcription factor regulating cell processes.
  • KLF4 has known tumor suppressive and oncogenic roles in various cancers.
  • The function of KLF4 in oral squamous cell carcinoma (OSCC) is not fully understood.

Purpose of the Study:

  • To investigate epigenetic alterations of KLF4 in oral cancer.
  • To elucidate the role of KLF4 in oral cancer carcinogenesis.
  • To understand the dual function of KLF4 in OSCC.

Main Methods:

  • Analysis of KLF4 expression in human oral cancer tissues and controls.
  • Assessment of KLF4 promoter methylation.
  • In vitro and in vivo experiments evaluating KLF4's effects on cell proliferation, apoptosis, migration, and invasion.
  • Investigation of mechanistic pathways involving MMP-9.

Main Results:

  • KLF4 expression is significantly decreased in oral cancer tissues.
  • KFL4 promoter hypermethylation correlates with reduced KLF4 expression.
  • KLF4 expression inversely correlates with tumor grade (lower in poorly differentiated tumors).
  • KLF4 inhibits proliferation, cell cycle progression, colony formation, and induces apoptosis.
  • KLF4 overexpression promotes migration and invasion; KLF4 knockdown inhibits these processes.
  • MMP-9 is implicated in KLF4-mediated cell migration and invasion.

Conclusions:

  • KLF4 exhibits a dual role in oral cancer, acting as both a tumor suppressor and an oncogene.
  • Epigenetic silencing via promoter hypermethylation contributes to KLF4 downregulation in OSCC.
  • KLF4's complex functions highlight its potential as a therapeutic target in oral cancer.
Keywords:
KLF4oncogeneoral squamous cell carcinomatumor suppressor

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