Emerging Role of Aurora A in Radioresistance: A Comprehensive Review

Abstract

Radiotherapy is one of the most conventional modes of treatment in several cancers. Failure of radiotherapy followed by acquisition of radioresistance is one of the emerging challenges faced by clinical experts. Unusual expression and functional implications of several molecules are observed to facilitate radioresistance. Aurora A, a member of the Aurora kinase (serine/threonine kinase) family, is one such molecule that shows significantly altered expression as well as non-canonical functional crosstalk with other associated factors (cell cycle regulators, signaling molecules, stemness markers, etc.) to favour the adaptations for the acquirement of radioresistance. These mechanisms include progression of cell cycle, stimulatory activation of factors by phosphorylation for enhancing the chance of cellular survivability, and prevention of apoptosis. This review article summarises how Aurora A is responsible for radioresistance in cancer and why this kinase should be considered a negative biomarker of radiosensitivity. This review discloses a wider opportunity in the field of research to find the mechanistic key regulatory pathway of Aurora A, which can be a potential target for enhancing the efficiency of treatment. Further investigations are required to explore the potential of Aurora A inhibitors as reliable radiosensitisers.