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Loss of KLF14 triggers centrosome amplification and tumorigenesis

Guangjian Fan1,2, Lianhui Sun1,2, Peipei Shan1,2

  • 1Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences, East China Normal University, Shanghai 200241, China.

Nature Communications
|October 7, 2015
PubMed

Insights

Loss of Kruppel-like factor 14 (KLF14) causes centrosome amplification, leading to cancer. Restoring KLF14 may offer a new therapeutic strategy for tumors.

Area of Science:

  • Cell Biology
  • Genetics
  • Oncology

Background:

  • Centrosome amplification is a hallmark of cancer, but its causes are not fully understood.
  • The Kruppel-like factor 14 (KLF14) gene's role in cancer development is largely unexplored.

Purpose of the Study:

  • To investigate the role of KLF14 in regulating centrosome duplication and tumorigenesis.
  • To explore the therapeutic potential of KLF14 in cancer treatment.

Main Methods:

  • Gene disruption in mice to study KLF14 function.
  • Molecular analysis of KLF14's interaction with Plk4.
  • Analysis of KLF14 and Plk4 expression in human cancer samples.
  • AOM/DSS-induced colon cancer model in mice.

Main Results:

  • KLF14 gene disruption in mice leads to centrosome amplification, aneuploidy, and spontaneous tumor formation.
  • KLF14 acts as a transcriptional repressor of Plk4, a key regulator of centrosome duplication.
  • KLF14 downregulation and Plk4 upregulation are observed in human cancers, with an inverse correlation in protein expression.
  • KLF14 depletion exacerbates chemically induced colon tumorigenesis.

Conclusions:

  • KLF14 functions as a tumor suppressor by inhibiting Plk4-mediated centrosome amplification.
  • Reduced KLF14 is a mechanism driving cancer development.
  • KLF14 represents a potential biomarker and therapeutic target for various cancers.

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