CDCA3 regulates the cell cycle and modulates cisplatin sensitivity in non-small cell lung cancer


Autoria(s): O'Byrne, K.; Adams, M.; Burgess, J.; Richard, D.
Data(s)

2016

Resumo

Cisplatin-based regimens are currently the most effective chemotherapy for non-small cell lung cancer (NSCLC). Cisplatin forms DNA crosslinks to stall DNA replication and induce apoptosis. However, intrinsic and acquired chemoresistance is a major therapeutic problem. We have identified ‘cell division cycle associated protein 3’ (CDCA3) as a novel protein that may prove useful in delaying or preventing cisplatin resistance in NSCLC. CDCA3 functions as part of an ubiquitin ligase complex to degrade the endogenous cell cycle inhibitors. While a role for CDCA3 in disease is emerging with elevated expression noted in oral squamous cell carcinoma, little else is known about CDCA3 or whether this protein may prove useful clinically.

Identificador

http://eprints.qut.edu.au/95259/

Publicador

Elsevier

Relação

DOI:10.1016/S1556-0864(16)30138-1

O'Byrne, K., Adams, M., Burgess, J., & Richard, D. (2016) CDCA3 regulates the cell cycle and modulates cisplatin sensitivity in non-small cell lung cancer. In European Lung Cancer Conference (ELCC 2016), 13 - 16 April 2016, Geneva, Switzerland.

Fonte

School of Biomedical Sciences; Faculty of Health; Institute of Health and Biomedical Innovation

Tipo

Conference Item