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Celecoxib, a selective cyclooxygenase-2 inhibitor, is known to possess anti-inflammatory activity and also induces apoptosis in various types of cancer cells. Here, we examined the molecular mechanism of celecoxib-induced apoptosis in cervical cancer cell lines (HeLa, CaSki and C33A). Screening of a cDNA microarray chip containing 225 different genes revealed thatGADD153(growth arrest and DNA damage inducible gene), a transcription factor involved in apoptosis, showed the strongest differential expression following celecoxib treatment in all three cervical cancer cell lines. Notably, siRNA-induced silencing of GADD153 suppressed celecoxib-induced apoptosis in all three cell lines, and exogenous expression ofGADD153triggered apoptosis in cervical cancer cells in the absence of other apoptotic stimuli. A luciferase reporter gene assay and mRNA stability tests revealed that the expression ofGADD153was regulated at both the transcriptional and post-transcriptional levels following celecoxib treatment. The region between −649 and −249, containing an intact C/EBP-ATF binding site, is required for celecoxib-induced stimulation ofGADD153promoter activity. In terms of signaling pathway, addition of the NF-κB inhibitor,N-tosyl-l-phenylalanyl-chloromethyl ketone, had no effect onGADD153expression levels. Celecoxib treatment induced Bak expression, whereas cell transfected with siGADD153 showed lower levels of celecoxib-induced Bak upregulation. These novel findings collectively suggest thatGADD153may play a key role in celecoxib-induced apoptosis in cervical cancer cells by regulating the expression of proapoptotic proteins such as Bak.

GADD153 mediates celecoxib-induced apoptosis in cervical cancer cells