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.