Global hypomethylation is a property of all cancers examined to date. Epigenetic states of
normal cells are greatly altered in cancer cells and that other epigenetic change. Cancer is now being viewed as a disease that involves both epigenetic and genetic changes that lead to alterations in gene expression. Mutations two types of genes that are thought to drive cancer: oncogenes and tumor suppressor genes. Tumor suppressor genes are normal genes that slow down cell division, repair DNA mistakes, or tell cells when to die (a process known as apoptosis or programmed cell death). When tumor suppressor genes don't work properly, cells can grow out of control, which can lead to cancer. An oncogene is a gene that has the potential to cause cancer. In tumor cells, they are often mutated or expressed at high levels. CpG islands (CGIs) are short interspersed DNA sequences that deviate significantly from the average genomic pattern by being GC-rich, CpG-rich, and predominantly nonmethylated. Most, perhaps all, CGIs are sites of transcription initiation, including thousands that are remote from currently annotated promoters. Shared DNA sequence features adapt CGIs for promoter function by destabilizing nucleosomes and attracting proteins that create a transcriptionally permissive chromatin state. Silencing of CGI promoters is achieved through dense CpG methylation. CGIs are therefore generically equipped to influence local chromatin structure and simplify regulation of gene activity.
In normal tissue, almost the entire genome is highly methylated with only CpG islands left unmethylated. In cancer cells, some CpG islands undergo de novo methylation.
If CpG islands are hypermethylated, how would this influence tumor supressor genes and oncogenes? Why would this lead to cancer?
Do you think the methylation could be reversed? What side effects could occur?
1.A gene which goes under hypermethylation that is essential for DNA(deoxyribonucleic acid) repair, result in deficient DNA... View the full answer