Apoptosis

Epigenetic mechanisms also play important roles in the regulation of apoptosis, a controlled form of cellular demise. Epigenetic mechanisms involving modifications to DNA and histone proteins can either activate or repress the expression of genes involved in apoptosis. DNA methylation involves the addition of a methyl group to cytosine residues in CpG dinucleotides and is frequently associated with gene silencing and can influence the expression of both pro-apoptotic and anti-apoptotic genes. For example, FAS (TNF receptor superfamily member 6) is a pro-apoptotic receptor that plays a role in the extrinsic form of apoptosis. In some cancer cells, the FAS promoter region becomes hypermethylated, resulting in reduced FAS expression. This epigenetic alteration can inhibit FAS-mediated apoptosis, allowing cancer cells to evade cell death. BCL2 is an anti-apoptotic gene that prevents cell death by inhibiting the mitochondrial apoptosis pathway. In certain cancers, the promoter region of BCL2 can become hypomethylated, leading to increased BCL2 expression and enhanced cancer cell survival. In addition to DNA methylation changes, epigenetic modifications of histone proteins, including acetylation and methylation, also play important roles in controlling apoptosis by regulating chromatin accessibility and transcription factor binding. For example, the anti-apoptotic gene BCL2 is regulated by histone acetylation. In cancer cells, the promoter region of BCL2 may show increased histone acetylation, leading to elevated BCL2 expression and enhanced cell survival. In addition, the tumour suppressor protein p53 plays a central role in apoptosis with its activation inducing apoptosis in response to DNA damage or other cellular stresses. Epigenetic modifications, including acetylation of specific lysine residues on histones associated with the p53 promoter region, can enhance the transcriptional activation of p53, leading to apoptosis. MiRNAs are small non-coding RNAs that can post-transcriptionally regulate gene expression. Epigenetic mechanisms can control the expression of miRNAs that target apoptosis-related genes. For example, miR-15a/miR-16-1 target the anti-apoptotic gene BCL2. In chronic lymphocytic leukaemia (CLL), the BCL2 gene is often overexpressed due to the loss of miR-15a and miR-16-1. Epigenetic silencing of the genomic loci encoding these miRNAs can therefore lead to increased BCL2 expression and reduced apoptosis. Long non-coding RNAs (lncRNAs) are RNA molecules that do not themselves code for proteins but can regulate gene expression of other proteins. Epigenetic changes can affect the expression of lncRNAs involved in apoptosis regulation. For example, the lncRNA H19 has been implicated in apoptosis control. In some cancers, aberrant DNA methylation of the H19 promoter region can lead to its overexpression, which may modulate apoptosis-related pathways. In some instances, H19 can act as a competitive endogenous RNA (ceRNA) for certain microRNAs (miRNAs). By sequestering miRNAs, H19 can indirectly affect the expression of genes involved in apoptosis. For example, H19 can compete miR-675, and this interaction can relieve the miR-675-mediated inhibition of pro-apoptotic genes. Thus, epigenetic mechanisms, including DNA methylation, histone modifications, miRNAs, and lncRNAs, play important roles in the regulation of apoptosis. Epigenetic alterations can influence the expression of pro-apoptotic and anti-apoptotic genes, contributing to cell survival or death decisions. We offer a wide product catalogue of research tools for studying apoptosis, including AKT1 antibodies, FLI1 antibodies, Survivin antibodies, pan-AKT ELISA Kits, and DNase I ELISA Kits. Explore our full apoptosis product range below and discover more, for less. Alternatively, you can explore our Nuclear product range.