Introduction: Epigenetics is the study of heritable, dynamic changes to the genome that take place without regard to the DNA sequence. Cohesive interactions with different enzymes and other molecular elements are necessary. Abnormal epigenetic changes can trigger genetic expressions at the wrong time and encourage the development of tumors. The epigenetic modifiers are becoming interesting targets in numerous cancer therapies since they are reversible and vulnerable to external influences. Numerous epi-drugs have recently been created and linked to clinical usage. Epi-drug use has demonstrated compelling outcomes, including enhancement of anti-tumor effects, overcoming drug resistance, and activation of the host immune response, whether used alone or in combination with chemotherapy or immunotherapy. The goal of this review was Epigenetic regulation in human cancer: the potential role of epi-drug in cancer therapy.
Methods: This study has written about Epigenetic regulation in human cancer: the potential role of epi-drug in cancer therapy from scientific databases such as Science Direct, Springer, Google Scholar, and PubMed
Results: Results indicated Epigenetic modification mechanisms Histone modifications, non-coding RNAs, and DNA and RNA methylations, which are thought to be the primary regulatory mechanisms throughout cancer, can be used to classify the epigenetic alterations into three major categories. Despite this, strong data suggests that using epi-drugs alone or in conjunction with other medications can enhance the anti-tumor efficacy. However, one should not undervalue the related issues. First off, there are still many epigenetic chemicals undergoing laboratory research. How to convert the efficacy in vitro at nanomolar-scale concentrations into well-tolerated and effective clinical use would be the main difficulty for those molecules. In various cancer cell lines, it has been discovered that MG98 effectively reactivates silenced TSGs via downregulating DNMT1 and exhibits an inhibitory effect on proliferation. However, in clinical trials, it did not provide a meaningful response.
Conclusion: As Summary, another difficulty with epi-drugs is their off-target effects. The mechanism underlying epigenetic regulation is unclear due to its complexity, dynamic nature, and interdependence. Currently, certain widely used epi-drugs, including VPA, have a history of producing unintended epigenetic alterations. To facilitate their use in clinical therapy, such epi-drugs must have a well-established safety profile. In the meantime, the development of resistance to some of the epi-drugs is posing a challenge. The PRC2 reduction shown in the resistant AML cells suggests that the targeted c-Myc expression may be recovered. Additionally, contributing to BETI resistance in triple-negative breast cancer (TNBC) is the hyperphosphorylation of BRD4.
Keywords: Epigenetic, cancer, epi-drug, cancer therapy