Understanding epigenetic regulation processes can provide light on the causes and treatments for cancer. Epigenetic regulation entails two steps: altering chromatin (the genetic material) and inserting nucleic acids. These two mechanisms are critical to understanding why some people develop cancer while others do not.

Studies of MYC at the molecular level have shown that it controls many different gene programs in healthy cells. Also, it plays a crucial role in maintaining how quickly tumors grow. These investigations show that MYC is essential for tumor initiation and growth control, and they also suggest that MYC may play a causative role in oncogenic reprogramming. Crucial is MYC's function in both pluripotency and apoptosis maintenance. It also plays an essential role in the reprogramming of cancer cells.

Studies have demonstrated that MYC is critical in the onset of basal-like breast cancers. This research revealed that MYC overexpression in mammary luminal epithelial cells facilitates the revival of a pluripotency-related transcriptional pathway. Overexpression of the oncogene MYC is a hallmark of basal-like breast cancers, suggesting that this expression pattern may promote carcinogenesis.

Multiple anti-cancer drugs concentrate on modifying DNA's methylation patterns. Epi-drugs is the term used to describe these medications. These medications have demonstrated encouraging anti-tumor effects in clinical studies. However, clinical use approval has yet to be granted for them.

A cell's epigenetic state determines whether or not it will live and divide. Environmental and physiological changes may cause shifts in the form of epigenetic markers. Cell death might occur if the cells cannot adjust to the new conditions.

Epigenetic alterations may be broken down into three categories: DNA methylation, histone modification, and control by non-coding RNAs. As a result of their interactions with other molecular components, these alterations can be undone. Such alterations are critical for the growth and spread of cancer.

Around 70% of CpG dinucleotides in the mammalian genome are methylated, making it the most prevalent epigenetic alteration. Gene silence occurs through DNA methylation, the covalent addition of methyl groups to the five positions of the cytosine pyrimidine ring.

Epigenetic control is an exciting prospective target for cancer therapy. It responds to external conditions and hence is dynamic and reversible. In this context, chromatin changes, DNA methylation, and the control of ncRNAs are all included. These alterations have been the focus of several investigations because of their possible significance in carcinogenesis in cancer.

BET proteins are essential for chromatin remodeling and have a role in gene expression. They control RNA polymerase II-dependent transcription by forming complexes with other proteins, such as histone deacetylases. In addition, they are recognized readers of histone acetyl-lysine. Homologous recombination–based DNA damage repair is another process that has been demonstrated to be regulated by BETs.

BETs have been the subject of many studies in the last several years due to their possible connections to cancer development. BRD4, a bromodomain-containing protein, and SLUG, an extra-terminal peptide, are two of the best-studied BET family members. In breast cancer cells, BRD4 and SLUG were revealed to have a role in controlling BRCAness induction treatment. Others oncogenes have also been shown to have these effects.

Angiogenesis and cancer cell proliferation are aided by inflammatory cells in the tumor microenvironment. Furthermore, cancer cells sabotage the immune system to promote tumor development. They create an inflammatory milieu by altering the structure of healthy tissue.

One of the critical chemokines in the tumor microenvironment is CXCL12. Various tumor-associated cells, such as fibroblasts, innate lymphoid cells, and tumor-associated macrophages, secrete CXCL12. High levels of CXCL12 expression are linked to a worse outcome in breast cancer.

Combining epi-drugs with standard cancer treatment is a potent strategy. Multiple studies have shown that epi-drugs work together to cure cancer effectively. Epi-drugs can potentially improve tumor inhibition beyond that of conventional anti-cancer therapies by targeting epigenetic changes. They are also convenient for multi-drug regimens since they aim at a particular body part.

The effectiveness of epi-drugs in the treatment of cancers is debatable. Evidence shows that they cause epigenetic changes that may result in acquired resistance. Thus, tests of such chemicals in humans are still in progress. Therefore, there is a demand for epi-drugs that have a clear safety record.