Research Highlight

Anti-inflammatory drug for cervical cancer

doi:10.1038/nindia.2012.7 Published online 19 January 2012

The non-steroidal, anti-inflammatory drug celecoxib helps kill cervical cancer cells through multi-pronged molecular action, primarily by suppressing the expression of viral oncoprotein E6, according to new research.

The drug was found to create an environment favourable for the tumour suppressor protein p-53, which triggers programmed cell death of human papilloma virus-18 (HPV-18)-infected cervical cancer cells.

The researchers found that the down-regulation of oncoprotein E6 and enzyme cycloxygenase-2 (COX-2) with the help of celecoxib led to the stabilization and functional maturation of p53 leading to death of cervical cancer cells.

E6 helps degrade the tumor suppressor protein p53. A functional p53-network is required to inhibit tumor formation and to make many standard anti-cancer therapies successful. Degradation of functional p53 by HPV-E6 hampers not only helps development of cervical cancer but also to worsens prognosis and treatment.

The study suggests that therapies designed to maneuver a functional pro-p53 network over an anti-p53-network could be successful in the management of virally infected cervical cancers.

The mechanism raises hopes for more efficient cervical cancer therapy, says lead scientist Tanya Das.


  1. Saha, B. et al. Restoration of tumor suppressor p53 by differentially regulating pro- and anti-p53 networks in HPV-18-infected cervical cancer cells. Oncogene 31, 173-186 (2012) | Article | PubMed |