Cell cycle inhibitors are components of the regulatory machinery that controls the cell cycle, helping to ensure that cell division occurs in a controlled manner. Epigenetic mechanisms, such as DNA methylation and histone modifications, play important roles in the regulation of cell cycle inhibitors. For example, p21 (CDKN1A) is a cyclin-dependent kinase inhibitor that halts cell cycle progression by binding to and inhibiting the activity of cyclin-CDK complexes. The promoter region of the CDKN1A gene, encoding p21, can undergo epigenetic modifications that impact its expression. DNA methylation of the CDKN1A promoter can silence the gene, leading to reduced p21 levels. In cancer cells, such hypermethylation of the CDKN1A promoter is a common mechanism for inactivating p21 and promoting uncontrolled cell proliferation. p16 (CDKN2A), also known as INK4A, is another important cyclin-dependent kinase inhibitor that inhibits cell cycle progression by preventing the phosphorylation of the retinoblastoma (Rb) protein. CDKN2A encodes two important tumour suppressor proteins, p16INK4a and p14ARF, which each play critical roles in regulating the cell cycle and preventing uncontrolled cell proliferation. Epigenetic silencing of the CDKN2A gene through promoter hypermethylation is a common event in many cancers. For example, in lung cancer, both non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC), frequently exhibit epigenetic silencing of CDKN2A via DNA hypermethylation. Additionally, histone modifications, such as histone deacetylation, can also contribute to CDKN2A silencing in lung cancer cells. When the CDKN2A promoter is hypermethylated, both p16INK4a and p14ARF expression are reduced, allowing cells to bypass the G1 checkpoint and continue cycling. This epigenetic alteration therefore contributes significantly to tumorigenesis. Similarly, p27 (CDKN1B) regulates the G1 to S phase transition by inhibiting cyclin-CDK complexes. Epigenetic mechanisms can also modulate p27 expression. In some cancer types, the promoter region of the CDKN1B gene is hypermethylated, resulting in reduced p27 expression, promoting uncontrolled cell proliferation, and contributing to tumorigenesis. Retinoblastoma protein (Rb) is a critical tumour suppressor protein that controls cell cycle progression by inhibiting the activity of E2F transcription factors, which regulate the expression of genes required for cell cycle entry and progression. As with cell cycle inhibitors, epigenetic modifications, such as hypermethylation of the RB1 gene promoter, can lead to the inactivation of the Rb protein in various cancers. Loss of Rb function allows cells to override cell cycle checkpoints and therefore continue dividing uncontrollably. miR-34a is a microRNA that targets multiple cell cycle regulators, including p53 and CDK4. Epigenetic silencing of miR-34a by promoter hypermethylation has been observed in various cancers, leading to dysregulation of the cell cycle and increased proliferation. Histone deacetylase (HDAC) inhibitors can restore the expression of silenced cell cycle inhibitors by altering histone acetylation patterns. For example, HDAC inhibitors can reactivate p21 and p27 expression in some cancer cells, leading to cell cycle arrest and apoptosis. Thus, epigenetic mechanisms, particularly DNA methylation and histone modifications, play important roles in the regulation of cell cycle inhibitors. We provide a large product range of research tools for studying cell cycle inhibitors, including p53 antibodies, p27 KIP 1 antibodies, p63 antibodies, p53 ELISA Kits, and p21 ELISA Kits. Explore our full cell cycle inhibitor product range below and discover more, for less. Alternatively, you can explore our p53, Cip & Kip, and INK4 product ranges.