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Unconventional Functions of Mitotic Kinases in Kidney Tumorigenesis

Pauline Hascoet1, Franck Chesnel1, Cathy Le Goff1

  • 1UMR 6290 (IGDR), CNRS, University Rennes-1 , Rennes , France.

Frontiers in Oncology
|November 19, 2015
PubMed

Insights

Aneuploidy, common in clear cell renal cell carcinoma (ccRCC), is linked to poor patient outcomes. This review explores the non-mitotic roles of specific kinases in ccRCC development and genetic instability.

Area of Science:

  • Oncology
  • Genetics
  • Cell Biology

Background:

  • Human tumors frequently display genetic alterations, including aneuploidy, which correlates with poor prognosis in various carcinomas like renal cell carcinoma (RCC).
  • Clear cell renal cell carcinoma (ccRCC), the predominant RCC subtype, is characterized by Von Hippel-Lindau gene dysfunction and genetic instability.
  • This instability may stem from disruptions in the cell cycle mitotic spindle checkpoint and involve Aurora kinases, crucial for centrosome maturation.

Purpose of the Study:

  • To review the unconventional, non-mitotic functions of specific kinases in renal tumorigenesis.
  • To elucidate the role of these kinases in the genetic instability and aneuploidy observed in ccRCC.

Main Methods:

  • Literature review focusing on the non-mitotic roles of Aurora kinases, polo-like kinase 1, casein kinase 2, and doublecortin-like kinase 1.
  • Analysis of existing research on genetic alterations and cell cycle regulation in renal cell carcinoma.

Main Results:

  • Aneuploidy in ccRCC is associated with poor patient outcomes.
  • Loss of cell-cell adhesion and apical-basal polarity, potentially regulated by mitotic kinases, contributes to aneuploidy.
  • The review highlights the "non-mitotic" functions of key kinases in renal tumorigenesis.

Conclusions:

  • Specific kinases play critical roles beyond mitosis in the development of ccRCC.
  • Understanding these unconventional functions is essential for comprehending ccRCC pathogenesis and genetic instability.
  • Further research into these kinase functions may reveal novel therapeutic targets for ccRCC.
Keywords:
Aurora-A kinasekidneymitotic kinasesnon-mitotic functionstumorigenesis

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