Role of the cyclin-dependent kinase inhibitors in the development of cancer

Down‐regulation of p27Kip1 expression is correlated with increased cell proliferation but not expression of p21waf1 and p53, and human papillomavirus infection in benign and malignant tumours of sinonasal regions

“…In resting cells, the level of p27 provides an inhibitory threshold above which G1 cyclins D/E/CDK accumulate before activation, while in cycling cells, this protein is sequestered by high levels of active cyclin D/CDK4 complexes and reduced by ubiquitin‐proteasome‐dependent degradation 4 , 18 , 19 . This study clearly demonstrated significantly decreased p27 expression in benign and malignant lesions of sinonasal tumours as compared to normal paranasal sinus epithelium.…”

Synergistic interaction of the histone deacetylase inhibitor SAHA with the proteasome inhibitor bortezomib in cutaneous T cell lymphoma

“…In addition, we showed that bortezomib and SAHA induced an upregulation of p21 and of p27 in consistence with findings in other entities. The CDK inhibitors p21 and p27, two members of the INK‐4 family, have been described as regulators of the cell cycle in normal and malignant lymphocytes (27, 28). P21 induces growth arrest by inhibiting the ability of the cyclin‐CDK complex to phosphorylate the cell cycle regulator Rb.…”

Histone deacetylase inhibitors reduce VEGF production and induce growth suppression and apoptosis in human mantle cell lymphoma

“…Treatment with NaB lead to an induction of p21 in two of three cell lines, while expression of p27 was not altered. The CDK inhibitors p21 and p27, two members of the INK‐4 family, have been described as regulators for cell cycle regulation in normal and malignant lymphocytes (36, 37), including MCL. P21 induces growth arrest by inhibiting the ability of the cyclin–CDK complex to phosphorylate the cell cycle regulator Rb.…”