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Suppression of Aurora-A oncogenic potential by c-Myc downregulation

Shangbin Yang1, Shun He, Xiaobo Zhou

  • 1State Key Laboratory of Molecular Oncology and Laboratory of Cell and Molecular Biology, Cancer Institute and Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

Experimental & Molecular Medicine
|October 5, 2010
PubMed

Insights

Aurora-A overexpression drives cancer by increasing c-Myc, a key oncogene. Inhibiting c-Myc reduces cancer growth and overcomes drug resistance, suggesting c-Myc as a therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Abnormalities in serine/threonine kinase Aurora-A are prevalent in various cancers.
  • Aurora-A's role in mitosis is established, but its specific contribution to tumorigenesis is not fully understood.

Purpose of the Study:

  • To elucidate the mechanism by which Aurora-A contributes to cancer development.
  • To investigate the relationship between Aurora-A and the oncogene c-Myc in tumorigenesis.

Main Methods:

  • Investigated the effect of Aurora-A overexpression on c-Myc expression and activity.
  • Utilized RNA interference to inhibit c-Myc expression and assess its impact on Aurora-A's oncogenic potential.
  • Evaluated the effect of c-Myc downregulation on cisplatin resistance in esophageal cancer cells.

Main Results:

  • Aurora-A overexpression was found to enhance both the expression level and transcriptional activity of c-Myc.
  • Inhibition of c-Myc significantly reduced cellular proliferation, transformation rates, and centrosomal aberrations induced by Aurora-A.
  • Downregulation of c-Myc effectively reversed Aurora-A-mediated resistance to cisplatin in esophageal cancer cells.

Conclusions:

  • c-Myc plays a crucial role in mediating the oncogenic activities of Aurora-A.
  • Targeting c-Myc represents a potential therapeutic strategy for cancers exhibiting Aurora-A overexpression.

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