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Exploring the role of epigenetics in cancer development, substance addiction, and learning and memory. Discover how DNA methylation and microRNA regulation contribute to gene expression changes in these conditions. The text delves into how these epigenetic modifications can lead to cancer progression, influence addictive behaviors, and form the molecular basis of memory in the brain.
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Aberrant methylation of CpG islands can lead to the silencing of tumor suppressor genes, contributing to the onset and progression of cancer
Dysregulation of microRNAs
In colorectal cancer, dysregulation of microRNAs can contribute to the silencing of tumor suppressor genes through CpG island methylation
In breast cancer, overexpression of microRNA-182 can suppress the expression of the BRCA1 gene, a crucial player in DNA repair, without altering its DNA methylation status
Addiction involves enduring behavioral changes that are underpinned by epigenetic alterations in the brain, including histone modifications, DNA methylation, and regulation by microRNAs
Altering gene expression of FosB
Psychoactive substances like nicotine and cocaine can trigger epigenetic changes in the brain, leading to altered expression of genes like FosB, which plays a pivotal role in the addictive process
While some epigenetic changes caused by smoking can be partially reversed after quitting, certain "molecular scars" may persist and contribute to the long-term consequences of addiction
DNA methylation is a key epigenetic mechanism that can be altered by experiences, such as learning and memory formation
Role of the hippocampus
Fear conditioning in rats can lead to changes in DNA methylation in the hippocampus, a brain region integral to memory
The activity of TET enzymes is crucial for the regulation of gene expression associated with learning and memory