Cancer Genetics and Epigenetics, 2025, Vol.13, No.2, 77-89 http://medscipublisher.com/index.php/cge 86 9 Concluding Remarks Histone modification is crucial for the deterioration and treatment of prostate cancer. These changes, such as acetylation, methylation, phosphorylation and ubiquitination, can alter the internal structure of the cell nucleus and the mode of gene activity, but do not change the DNA itself. Abnormal histone modifications are associated with the misfunctioning of some important genes, which are responsible for cells' DNA repair, control of the growth cycle, determination of death, and intercellular adhesion. For instance, an increase in the three methyl groups at site 27 of histone H3 (often caused by an excessive amount of EZH2 protein) involves the occurrence of prostate cancer. In addition, the loss of acetyl and methyl groups in histones can also affect the function of androgen receptors (which are very important for the development of prostate cancer). These epigenetic changes not only assist in tumor formation but may also serve as markers for diagnosis and assessment of the condition, as well as targets for treatment. Therapeutic approaches targeting histone modification (epigenetic therapy) hold great promise in improving the outcome of prostate cancer. Because histone changes can be restored, this makes them ideal therapeutic targets. Inhibitors such as HDAC (histone deacetylase) and HMT (histone methyltransferase) have been proven to reactivate those repressor genes that have been turned off, making cancer cells more likely to be killed by therapies such as radiotherapy. For example, HDAC inhibitors can not only activate genes, but also control cell death and enhance the effect of radiotherapy. At present, the efficacy of these drugs on patients with prostate cancer is under clinical testing, and some have shown results in animal studies. Developing new drugs that can simultaneously act on multiple epigenetic changes is also an effective way to improve therapeutic effects and prevent drug resistance. The future of epigenetic treatment for prostate cancer is bright, but it also faces difficulties. An important opportunity is to develop more precise inhibitors specifically targeting certain histone changes or related enzymes. This precise performance reduces adverse reactions and enhances therapeutic effects. Furthermore, the combined use of epigenetic therapy with other treatments (such as drugs that interfere with cell communication or chemotherapy) may enhance the effect and defeat the resistance of cancer cells to drugs. However, challenges still exist, such as clarifying the complex interrelationships among different epigenetic changes and finding reliable identification markers to distinguish which patients are suitable for which therapy. More research is needed to clarify the specific processes of these changes and to confirm the actual benefits of epigenetic therapy in more diverse patients. Acknowledgments Thank you to the peer review for critically reading the manuscript and providing suggestions for improvement. Conflict of Interest Disclosure The authors affirm that this research was conducted without any commercial or financial relationships that could be construed as a potential conflict of interest. References Balaji A.K., Saha S., Deshpande S., Poola D., and Sengupta K., 2022, Nuclear envelope, chromatin organizers, histones, and DNA: the many achilles heels exploited across cancers, Frontiers in Cell and Developmental Biology, 10: 1068347. https://doi.org/10.3389/fcell.2022.1068347 Baumgart S.J., and Haendler B., 2017, Exploiting epigenetic alterations in prostate cancer, International Journal of Molecular Sciences, 18(5): 1017. https://doi.org/10.3390/ijms18051017 Bannister A.J., and Kouzarides T., 2011, Regulation of chromatin by histone modifications, Cell Research, 21(3): 381-395. https://doi.org/10.1038/cr.2011.22 Burlibașa L., Nicu A.T., Chifiriuc M.C., Medar C., Petrescu A., Jinga V., and Stoica I., 2023, H3 histone methylation landscape in male urogenital cancers: from molecular mechanisms to epigenetic biomarkers and therapeutic targets, Frontiers in Cell and Developmental Biology, 11: 1181764. https://doi.org/10.3389/fcell.2023.1181764 Campos E.I., and Reinberg D., 2009, Histones: annotating chromatin, Annual Review of Genetics, 43: 559-599. https://doi.org/10.1146/annurev.genet.032608.103928 Chen Z., Wang L., Wang Q., and Li W., 2010, Histone modifications and chromatin organization in prostate cancer, Epigenomics, 2(4): 551-60. https://doi.org/10.2217/epi.10.31
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