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PLK4 overexpression and its effect on centrosome regulation and chromosome stability in human gastric cancer

Kazuya Shinmura1, Nobuya Kurabe, Masanori Goto

  • 1Department of Tumor Pathology, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi Ward, Hamamatsu, Shizuoka, 431-3192, Japan, kzshinmu@hama-med.ac.jp.

Molecular Biology Reports
|July 2, 2014
PubMed

Insights

Polo-like kinase 4 (PLK4) is upregulated in gastric cancer, driving centrosome amplification and chromosome instability. This suggests PLK4 plays a role in gastric cancer development and progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Polo-like kinase 4 (PLK4) is a key regulator of centrosome duplication.
  • Centrosome abnormalities are implicated in cancer development.
  • The role of PLK4 in gastric cancer remains largely unexplored.

Purpose of the Study:

  • To investigate the involvement of genetic abnormalities of PLK4 in human gastric cancer.
  • To determine PLK4 mRNA expression levels in gastric cancer cell lines and primary tumors.
  • To elucidate the functional consequences of PLK4 overexpression in gastric cancer cells.

Main Methods:

  • RT-PCR analysis to assess PLK4 mRNA expression in gastric cancer cell lines and primary tumors.
  • Identification of PLK4 variants using molecular techniques.
  • Establishment of inducible PLK4-expressing AGS gastric cancer cells.
  • Immunofluorescence and FISH analyses to evaluate centrosome amplification and chromosome instability.
  • Assessment of primary cilia formation.

Main Results:

  • PLK4 mRNA was upregulated in 57.1% of gastric cancer cell lines and 50.0% of primary gastric cancers (P=0.0139).
  • A novel PLK4 variant lacking exon 5 was identified.
  • PLK4 overexpression induced centrosome amplification and chromosome instability in AGS cells.
  • PLK4 overexpression suppressed primary cilia formation.

Conclusions:

  • PLK4 is upregulated in a subset of human gastric cancers.
  • PLK4 overexpression contributes to centrosome amplification and chromosome instability.
  • PLK4 dysregulation may play a significant role in gastric carcinogenesis.
  • PLK4 may impact primary cilia formation, a process relevant to cell signaling and development.

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