Depletion of the cdk Inhibitor p16INK4a Differentially Affects Proliferation of Established Cervical Carcinoma Cells

Infections with high-risk human papillomaviruses (hrHPV) contribute to cervical carcinoma. The cdk inhibitor and tumor suppressor p16(INK4A) is consistently upregulated in cervical carcinoma cells for reasons that are poorly understood. We report here that downregulation of p16(INK4A) gene expression in three different cervical carcinoma cell lines reduced expression of the E7 oncogene, suggesting a positive feedback loop involving E7 and p16(INK4A). p16(INK4A) depletion induced cellular senescence in HeLa but not CaSki and MS-751 cervical carcinoma cells.