Final answer:
Histone acetylation can lead to the activation of proto-oncogenes, potentially resulting in uncontrolled cell proliferation and the development of cancer; in particular, changes in acetylation may influence the activity of tumor suppressor genes like p53, associated with cancer when mutated.
Step-by-step explanation:
In the context of cancer and epigenetic alteration, histone acetylation plays a critical role in the regulation of gene expression. Acetylation of histone proteins typically reduces their positive charge, leading to a less compact and more transcriptionally active chromatin structure. This can result in increased expression of genes, including those involved in cell growth and proliferation. When histone acetylation occurs on proto-oncogenes, which are genes that in their normal state help regulate cell growth, it can lead to their overactivation.
If these proto-oncogenes are overexpressed, they can function as oncogenes, promoting uncontrolled cell proliferation and the development of cancer. Unregulated cell division is a hallmark of cancer, and it is often caused by mutations or epigenetic changes that activate proto-oncogenes or inactivate tumor suppressor genes like p53. In summary, alterations in histone acetylation can significantly impact gene expression, which in turn can contribute to oncogenesis if the balance of cell cycle regulation is disrupted.