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Aurora-A: a potential DNA repair modulator
Yan Wang1, Huizhen Sun, Ziliang Wang
1Cancer Institute, Fudan University Shanghai Cancer Center, 270 Dong'an Road, Shanghai, China, wangxyyan@sina.com.
Abstract:
It is well-known that overexpression of Aurora-A promotes tumorigenesis, but the role of Aurora-A in the development of cancer has not been fully investigated. Recent studies indicate that Aurora-A may confer cancer cell chemo- and radioresistance through dysregulation of cell cycle progression and DNA damage response. Direct evidences from literatures suggest that Aurora-A inhibits pRb, p53, p21(waf1/cip1), and p27(cip/kip) but enhances Plk1, CDC25, CDK1, and cyclin B1 to repeal cell cycle checkpoints and to promote cell cycle progression. Other studies indicate that Aurora-A suppresses BRCA1, BRCA2, RAD51, poly(ADP ribose) polymerase (PARP), and gamma-H2AX to dysregulate DNA damage response. Aurora-A may also interact with RAS and Myc to control DNA repair indirectly. In this review, we summarized the potential role of Aurora-A in DNA repair from the current literatures and concluded that Aurora-A may function as a DNA repair modulator to control cancer cell radio- and chemosensitivity, and that Aurora-A-associated DNA repair molecules may be considered for targeted cancer therapy.
Insights
Aurora-A overexpression promotes cancer. This review explores its role in DNA repair, showing it modulates cancer cell sensitivity to chemotherapy and radiation, suggesting Aurora-A targets for therapy.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Overexpression of Aurora-A kinase is linked to tumorigenesis.
- Its precise role in cancer development, particularly in chemo- and radioresistance, requires further investigation.
- Aurora-A influences cell cycle progression and DNA damage response pathways.
Purpose of the Study:
- To review and summarize the current literature on the role of Aurora-A in DNA repair.
- To elucidate the mechanisms by which Aurora-A affects cancer cell sensitivity to therapeutic agents.
- To identify potential therapeutic targets associated with Aurora-A in cancer treatment.
Main Methods:
- Literature review of existing studies on Aurora-A.
- Analysis of Aurora-A's interactions with cell cycle regulators (e.g., pRb, p53, CDK1, cyclin B1).
- Examination of Aurora-A's impact on DNA damage response proteins (e.g., BRCA1, BRCA2, PARP, gamma-H2AX).
Main Results:
- Aurora-A dysregulates cell cycle checkpoints by inhibiting inhibitors (pRb, p53, p21, p27) and enhancing activators (Plk1, CDC25, CDK1, cyclin B1).
- Aurora-A suppresses key DNA repair proteins including BRCA1, BRCA2, RAD51, PARP, and gamma-H2AX, thereby impairing DNA damage response.
- Evidence suggests Aurora-A indirectly influences DNA repair through interactions with RAS and Myc.
Conclusions:
- Aurora-A acts as a modulator of DNA repair processes in cancer cells.
- Its activity influences cancer cell radio- and chemosensitivity.
- Aurora-A-associated DNA repair molecules represent promising targets for novel cancer therapies.
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