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Introduction Cancer is a major global health concern, responsible for approximately 10 million deaths in 2020, representing nearly one-sixth of all deaths worldwide. In general, breast, lung, colorectal, and prostate cancers are among the most prevalent types worldwide. Cancer rises from the uncontrolled proliferation of mutated somatic cells. These cells have special features that allow them to reduce the period of the cell cycle and evade the immune system. Oncogenes are genes that lead to cancer. Originally found in viruses, many of its counterparts ended up in the human genome as proto-oncogenes, which promote normal growth and division of cells. Genetic alterations that promote the formation of oncogenes from proto-oncogenes belong to mainly four categories, those are epigenetic changes, point mutations, gene amplification and translocations. To begin with, the alteration of chromatin structure caused by epigenetic changes may serve to alter gene expression. For instance, acetylation by histone acetyltransferases loosens the chromosome and neutralises the charges on DNA to tune expression to an extremely high level. Such modification on a proto-oncogene would severely boost expression, turning it into an oncogene. On the other hand, point mutations alter one digit in the cell genome. For proto-oncogenes, a change within the promoter and enhancer region, which normally regulates expression, may alter gene regulation, causing it to be over-expressed and become an oncogene. Apart from slight changes in the genome, chromosomal translocation and duplication often rearrange a section of the chromosome. For example, translocation occurs when two sections of non-homologous chromosomes swap place, while duplication inserts a copy of an existing gene to that locus. In effect, if the translocated region contains a proto-oncogene and is placed near an active promoter, the genes are overexpressed; similarly, duplication causes gene expression to double which amplifies gene product. Namely, chronic myelogenous leukemia (CML) results from the translocation between chromosome 22 and 9 in white blood cells during mitosis, leading to uncontrolled cell cycle progression. Unlike genes, which are sequences encoded by nucleotides that form the chromosome by wrapping around histones. The epigenome is represented by modifications on the nucleotides and histones that do not alter the genetic sequence of the cell. Typical modifications associated with gene expression include DNA methylation and histone modifications. The two modifications differ in the location of the modification and their effects on transcription. DNA methylation is represented by the addition of methyl groups(-CH3) on the cytosine bases. The addition of methyl groups is carried out by DNA methyltransferases and its removal is catalysed by DNA demethylases. Overall, methyl groups are the promoter and enhancer regions that act as barriers that prevent the binding of protein complexes containing transcription factors and polymerases, thereby reducing transcription. They are frequently found in genes, especially the promoter regions, that are silenced or less expressed than others, as well as on inactivated X chromosomes in females. Unlike methylation which applies on the nucleotides, modifications are also applied on histone proteins, thanks to its unique histone tail that protrudes outward. Multiple organic groups are addible to the histone tail, including acetyl, methyl and phosphate groups. Generally, the addition of acetyl groups is found to neutralise the charge around histone molecules, leading to a loosened chromosome on which molecules can more easily bind and start transcription. The addition of acetyl groups and catalysed by histone acetyltransferases and its removal is catalysed by Histone deacetylases. Conversely, the addition of methyl groups on histones is observed to decrease transcription by tightening the chromosomes around histones, making it harder for transcription factors to bind to it. Compared to genetic mutations, epigenetic modifications are reversible by exposure to related enzymes, causing it to be a promising approach to alter high expression caused by cancer in a short period. Factors that increase the rate of mutation and promote cancer are called carcinogens, alcoholics, tobacco and air pollution are all known risk factors for oncogene formation. They account for approximately one-third of cancer-related deaths. Chronic infections also contribute to cancer risk, particularly in less economically developed countries (LEDCs). In 2018, approximately 13% of globally diagnosed cancers were linked to carcinogenic infections including hepatitis B virus (HBV), hepatitis C virus (HCV) and human papillomavirus (HPV). In LEDCs, infections like human papillomavirus (HPV) are responsible for about 30% of cancer cases. Effective detection and treatment can lead to successful cures for many cancers. Standard treatments for localized prostate cancer, stages I-III, include active surveillance, radical prostatectomy and radiotherapy. For men with recurrent prostate cancer, options include chemotherapy, radiotherapy, and androgen deprivation therapy (ADT). To begin with, active surveillance involves closely monitoring cancer with a plan to treat it if it shows signs of growth. It is often used for small, non-metastatic, or slow-growing cancers in the very low, low, or favourable intermediate-risk group. Benefits include retaining the normal function of the male gonad, lowering the cost of treatment, and avoiding unnecessary treatment. However, disadvantages include the risk of cancer spreading before treatment, missed opportunities for a cure, increased patient anxiety, and frequent medical checks. In addition, radiotherapy is a highly effective treatment for prostate cancer. Cancer cells are destroyed by high doses of radiation, delivered to the cancerous cells using techniques such as brachytherapy and external beam radiation therapy (EBRT). Brachytherapy involves transferring radioactive sources into the prostate gland. EBRT uses strong X-ray beams to target prostate tissues specifically. This technique outweighs surgical therapy in a significant aspect, as it often results in fewer risks such as bleeding, heart attack, blood clots, urinary incontinence, and erectile dysfunction. Furthermore, radical prostatectomy is the surgical removal of the prostate gland, performed through open or laparoscopic surgery. It is typically done for more severe cancer cases. Moreover, hormonal therapy, or androgen deprivation therapy (ADT), is used to treat advanced or metastatic prostate cancer. It works by blocking the production of testosterone and other male hormones, which can fuel prostate cancer cells. However, ADT can lead to adverse effects including high cholesterol, fatigue, bone loss, heart disease, anaemia, etc. Last but not least, chemotherapy uses drugs to kill or slow the growth of cancer cells. Docetaxel is a standard first-line therapy for castration-resistant prostate cancer. It is an antimicrotubular agent that binds to β-tubulin, inhibiting microtubule depolymerization, suppressing cell division, and triggering cell death. Research is also being conducted on traditional medicine, nanotechnology, and gene therapy to improve prostate cancer treatment, overcome drug resistance, and reduce side effects. Methodology Throughout my research, I gathered my sources from authoritative databases including PubMed by the National Institution of Health, Elsevier ScienceDirect, and influential textbooks from world-leading universities including Molecular Biology of the Cell and Campbell Biology. During my indexing, I used the queries of “Prostate Cancer AND Epigenetic Changes”, “Prostate Cancer AND Treatments” and “Prostate Cancer AND Treatments AND Resistance” as well as keywords including prostate cancer, DNA methylation, histone modifications, epigenetic drugs, DNMT inhibitors and HDAC inhibitors. After selecting and filtering valid and appropriate articles including literature reviews and experimental studies, I read them thoroughly and highlighted key phrases to be implemented and cited in this research essay. Only articles written in English were collected. This elicited one of the main limitations in my methodology, that is, the lack of first-hand resources in comparison to many existing experimental studies conducted by more acknowledged professionals. Another limitation of my methodology is the limited access to sources from more recent journals, conferences and confidential research. However, I still managed to integrate the experimental results from multiple studies and papers to reach my conclusion. I use the Vancouver format for my citation as it is one of the major formats used for studies including biological sciences and medicines. Epigenetic Changes in Prostate Cancer Behind lung cancer, prostate cancer is the second-leading cancer in America. According to the American Cancer Society, prostate cancer accounts for the death of 1 in 44 men. In general, histone acetylation and DNA methylation are the main epigenetic changes commonly detected in prostate cancer cells. They function either individually or collectively in the progression of cancer tumours (1). However, the reversibility of alterations in the epigenome created potential treatment methods that seek to reform the epigenome in normal cells, thereby reactivating silenced or silencing overexpressed genes. Several aberrations in the prostate epigenome include DNA hypermethylation, hypomethylation, and histone acetylation. To begin with, DNA hypermethylation is one of the most commonly investigated epigenetic aberrations in cancer. Dating back to as far as 2005 Li LC et al. obtained 52 articles reporting over 30 hypermethylated genes in prostate cancer (1). Within hypermethylated genes, silencing of cell-cycle control genes, DNA damage repair genes and hormone response genes are established important roles in prostate cancer development. Cancer tumours are often the result of the unregulated proliferation of cancer cells, in which the period of the cell cycle is reduced to increase the rate of cell division. Conventionally, checkpoints are located at the end of every phase to ensure the functionality of the cells by arresting the cell cycle when abnormalities such as DNA damage are presented. The cell checkpoints are regulated by intricate modulation systems, one of the modulators in retinoblastoma (RB1) protein (38). Thus, silencing of cell-cycle control genes by hypermethylation enables malfunctioning cancer cells to skip checkpoints that ensure their integrity, which can be achieved by tumour suppressor genes. Their product arrests the cell cycle when severe DNA damage occurs. The initial tumour suppressor gene to be discovered was RB1, and alterations in this gene have been detected in numerous types of tumours, including prostate cancer (2). However, the reason behind RB1 inactivation is ultimately found to be a result of mutation instead of hypermethylation (3)(39). Another type of tumour suppressor gene are CDKIs which obstruct the binding of RNA polymerase to the promoter region, thereby repressing transcription. Changes in CDKI expression are also reported to be responsible for cell cycle arrest (4, 5), and methylation-induced inactivation of the CDKN2A gene has been documented in prostate cancer cell lines and tissues (6)(40). DNA repair is a crucial mechanism that ensures the completeness and integrity of the cell genome during replication. Aberrations in DNA damage repair genes may lead to a higher rate of faulty mutation which leads to cell proliferation. Hypermethylation on two DNA repair genes have been observed in prostate cancer cells: GSTP1, a detoxifier gene and MGMT, another DNA repair gene. GSTP1 is a gene responsible for carcinogen detoxification (7). In prostate cancer, methylation of the GSTP1 gene promoter is the most commonly observed epigenetic change, occurring in a frequency from 70% to 100% of prostate cancer DNA samples (8-10). MGMT reduces alkyl adducts from the genome, it also repairs DNA thereby preventing point mutations. Tumours with deficient MGMT expression are more prone to point mutations in the genes that encode p53 and K-ras, potentially impacting the progression of cancer. Unlike hypermethylation which silences genes, hypomethylation involves the demethylation of conventionally methylated genes, leading to an overexpression of some genes. Hypomethylation could be separated into two major groups, those are global and gene-specific hypomethylation. Global hypomethylation represents a general decrease in methylation levels across the entire genome of a cell or tissue. In 1987, Bedford et al. found that the methylation content in DNA from metastatic tumours was significantly lower compared to nonmetastatic prostate tumours. Gene-specific hypomethylation, however, represents a reduction in DNA methylation levels at specific gene loci or promoters, rather than affecting the entire genome. In prostate cancer, the PLAU gene, which encodes a tumour-promoting protein and is conventionally methylated, is found to be heavily expressed and promotes cell proliferation (11). Histone modifications such as histone acetylation are also important regulators of gene expression in the epigenome. Coxsackie and adenovirus receptor (CAR) is a receptor for adenoviruses and their identification. Reduced expression of the CAR gene has been observed in prostate cancer and is correlated with higher Gleason scores (12). In urogenital cancer cells, such as the PC-3 prostate cancer cell line, histone acetylation regulates the activation of the CAR gene, which can be stimulated by depsipeptide, an inhibitor of histone deacetylases (HDACs)(13). Histone methylations, though rare, are also present in prostate cancer. In the prostate cancer cell line LNCaP, methylation of H3 at lysine 4 is linked to the silencing of the prostate-specific antigen (PSA) gene. Additionally, transcription of the PSA gene mediated by the androgen receptor (AR) is associated with a rapid reduction in di- and trimethylated H3 at lysine 4(41). Apart from functioning separately, sufficient evidence has reported that DNA methylation and histone modifications work together to decrease gene expression, by establishing a chromosome that is inactive in transcription as a result of binding to methylated DNA binding proteins like MeCP2. This binding subsequently attracts HDAC activity to methylated promoters, leading to the decrease in gene expression. In prostate cancer cells, DAB2IP expression is activated by the interaction between 5-aza-deoxycytidine, a demethylating agent, and trichostatin A (TSA), an HDAC inhibitor (42). Furthermore, DNA methylation and histone methylation may also cooperate to regulate gene expression. In LNCaP cancer cells, the silencing of the GSTP1 gene involves a series of sequential changes, starting with DNA methylation, followed by histone deacetylation and then histone methylation (14, 15). Epigenetic Treatments for Prostate Cancer Epigenetic modifications are best known for their specificity and reversibility. Throughout decades, their specificity has provided effective prostate cancer detection and classification (1), and their reversibility has offered many solutions that involve the mechanism of targeting potential biomarkers to up or down-regulate gene expression. The core of epigenetic treatments serves to reverse the abnormal modifications in the genome detected in prostate cancer cells, namely DNA hypermethylation, hypomethylation, and histone acetylation so that their function can be retained. To begin with, recovering the original epigenome from hypermethylation may require one of two methods, either inhibiting DNA methyltransferases or exposing the epigenome to known demethylating agents. 5-Azacytidine and 5-aza-deoxycytidine, or decitabine, serve as an inhibitor of DNA methyltransferases and it is one of the earliest inhibitors discovered. In 2014, Naldi et al. developed a brand-new drug-delivering pathway, by encapsulating decitabine in EMHVs (elastin-like polypeptide-modified hyaluronic acid nanoparticles) and further demonstrated a remarkable reduction in tumour mass in prostate cancer xenograft models (16). Furthermore, similar effects occurred on one of the highly aggressive forms of prostate cancer named neuroendocrine prostate cancer (NEPC), in which DNA methyltransferases (DNMTs) are found at elevated levels as a result of DNA hypermethylation and are strongly associated with tumour progression and metastasis. In a study conducted in November 2023, Yamada and colleagues investigated the effects of decitabine in NEPC using mouse models. They confirmed that treatment with decitabine showed promise in reducing tumour growth in both NEPC and RB1-deficient castration-resistant prostate adenocarcinoma (CRPC) models corresponding to their control group, that mice with DNMT genes knocked down also experienced reduced tumour development and metastasis. In addition, the study also introduced that decitabine treatment may lead to an increase in the expression of B7 homolog 3 (B7-H3), a protein that is typically expressed at low levels in prostate cancer cells. The researchers combined decitabine treatment with DS-7300a, an antibody-drug conjugate designed to specifically target B7-H3 and demonstrated a potential new treatment strategy for prostate cancer tumours (17). Apart from recovering from hypermethylation, DNA could also be methylated to reverse hypomethylation. Prior research pointed out that a novel type of short nucleotide called methylated sense oligonucleotide can alter DNA methylation in a sequence-specific manner both in lab and natural conditions. This method involves a synthetic oligonucleotide that has 5-methylcytosine instead of cytosine. When the methylated sense oligonucleotide binds to one DNA strand, it creates a hemi-methylated DNA intermediate that is favoured by DNMTs that further methylate the other strand and extend the methylation around the target site. Using this technique, a methylated sense oligonucleotide that targets the promoter of the ESR2 gene was introduced into PC-3 prostate cancer cells, leading to site-specific methylation and silencing of ESR2 gene expression, which is upregulated in metastatic prostate cancer due to a demethylated promoter (18). In addition, some treatments also involved the recovery of the cell from histone acetylation. This may be achieved by either inhibiting histone deacetylase activity or exposing the epigenome to known acetylating agents such as histone acetyltransferases. Histone deacetylase inhibitors block the activity of HDAC to prevent potential deacetylation, thereby increasing gene expression. Histone deacetylases (HDACs) are crucial in driving prostate cancer progression. They are involved in a transcriptional co-repressor complex that impacts several tumour suppressor genes. Given their pivotal role in cancer, HDAC inhibitors are emerging as a promising class of chemotherapeutic agents. These inhibitors have demonstrated the ability to halt cell growth, promote differentiation, and induce apoptosis in prostate cancer cells (19). Sato et al. investigated the impact of the HDAC inhibitor OBP-801 on AR expression and tumour cell growth in prostate cancers. They found that OBP-801 treatment effectively inhibited the growth of three prostate cancer cell lines (22Rv1, VCaP, and LNCaP) and reduced AR expression by posttranscriptional regulation, irrespective of their hormone sensitivity. In a rat model of AR-dependent prostate tumorigenesis, treatment with OBP-801 significantly increased miR-320a expression, which was high in normal human prostate luminal cells but low in prostate cancer cells, and suppressed prostate tumorigenesis (20). Most HDAC inhibitors serve to increase gene expression and they encourage the expression of genes that suppress tumours and arrest the cell cycle. Trichostatin A (TSA), sodium butyrate (21), and valproic acid are among some of those (22). For instance, sodium butyrate and TSA enhance the inhibitory effect of 1,25-(OH)2-vitamin D3 on prostate cancer tissue growth by initiating programmed cell death (23), and valproic acid causes prostate cancer cell apoptosis by upregulating several genes that promote cell death (22). However, other HDAC inhibitors include depsipeptides such as romidepsins which decrease transcription. Depsipeptides reduce PC-3 cell growth by downregulating VEGF mRNA expression even though they cause acetylated histones to accumulate in the chromatin near the VEGF gene promoter (24). Romidepsin, by blocking HDAC1 and HDAC2, can trigger apoptosis, cell cycle arrest, and DNA damage in prostate cancer cells (25). It can also prevent tumour growth and metastasis in prostate cancer animal models. Vorinostat is another small molecule inhibitor that belongs to dicarboxylic acid diamide and targets both class I and II histone deacetylases (HDACs). Studies have demonstrated its efficacy in inhibiting the growth of human prostate cancer cell lines, including PC-3, DU-145, and LNCaP. Additionally, vorinostat has been shown to suppress the growth of PC-3 xenograft tumours in preclinical models (23). To supplement, the thesis of epigenetic modifications in cancer treatments lies not only in reversing aberration observed in cancerous cells but also in coping readily with other existing cancer treatments such as radio and chemotherapy. For example, one of the factors that may influence the development of radioresistant traits in prostate cancer cells is the epigenetic modification of their chromatin structure and gene expression. In addition, the enhanced ability of these cells to repair DNA damage caused by ionizing radiation and the disruption of their normal cell cycle checkpoints also reduce their sensitivity to radiotherapy (26). Therefore, specific targetable epigenetic molecules may overcome and predict PCa radio resistance by targeting the locus specified to that region. In conclusion, the flexibility and reversibility of epigenetic modifications have made epigenetic treatments a promising cancer treatment method. It had already shown its potential from existing drug treatments by either reversing the epigenome or providing modifications that counteract the effect of genetic mutations on regulatory genes and promoter regions. With enhanced delivery techniques and targeting, epigenetic drugs are now prominent in medical research. Data Analysis There have been multiple clinical trials since the beginning of the decade, yet all of them were carried out on a small scale. In general, less progress has been observed with trials using DNMT inhibitors than those using HDAC inhibitors. In a phase II trial (NCT00384839) evaluating 5-azacytidine, 36 patients with prostate cancer (PCa) were enrolled. Among them, 19 patients exhibited a PSA-doubling time (DT) of less than 3 months. The median PSA-DT for all patients was extended compared to baseline, increasing from 1.5 months to 2.8 months. Out of the participants, only one patient demonstrated a notable 30% decline in PSA levels, while 14 patients exhibited only a marginal decrease in PSA levels (44). For a trial on the efficiency of Panobinostat (LBH589), docetaxel and prednisone, castration-resistant prostate cancer (CRPC) patients were administered oral Panobinostat at a dosage of 20 mg/m^2, specifically on days 15 of two-week cycle, for a total of two cycles in one arm of the study and patients in the other arm were given a combination therapy consisting of oral Panobinostat at a reduced dosage of 15 mg/m^2, along with intravenous docetaxel at a dose of 75 mg/m^2. Additionally, oral prednisone was administered twice daily at a dose of 5 mg throughout the 21-day cycle. Both arms aimed to assess the efficacy and safety profile of the respective treatment regimens in patients diagnosed with CRPC. The combination of Panobinostat with docetaxel and prednisone in CRPC patients led to notable toxicity, primarily presenting as dyspnea and neutropenia. However, despite these adverse effects, 63% of patients experienced a significant decline (>50%) in prostate-specific antigen (PSA) levels (43). In a study utilizing propensity-matched cohorts comprising 879 chemotherapy-exposed patients and 1611 chemotherapy-naïve patients, the overall survival rates at 18 and 30 months were found to be 76.3% versus 70.5% and 61.6% versus 56.0%, respectively. These findings indicate only a slight alleviation for chemotherapy-exposed patients in terms of overall survival compared to chemotherapy-naïve patients (28). In another chemotherapy phase II trial in 2021, 100 patients underwent cabazitaxel at a dosage of 20 mg/m2 every three weeks for up to ten cycles. The primary endpoint was the rate of PSA response. Among the participants, 65 out of 99 (66%) experienced a reduction in PSA levels of 50% or more from baseline (29). As a result, the effect of epigenetic treatments seems to already reach similar effects in comparison to chemotherapies, despite a small scale of clinical trials, thereby illustrating its potential as a rising treatment scheme. Advantage and Limitations Epigenetic treatments are a novel approach that focuses on reversing the epigenome of the patients to reverse the effect brought up by cancerous mutations. In general, the advantages and potential of epigenetic treatments include their reversibility, precision, and increased sensibility by synergistic effects. To begin with, the reversibility of epigenetic modifications allows a complete reversal of epigenetic aberrations to transform cells back to their normal expression level. From one perspective, the reversibility simplifies the approaches to cancer treatments, that is, releasing corresponding medications that serve to reverse epigenetic aberrations at certain biomarkers. Meanwhile, reversibility also increases the fault-tolerance level for treatments. For instance, enzymes and inhibitors could be applied to correct the changes even if off-target effects are observed since the base sequence of the genome is not altered. In addition, epigenetic treatments bear a higher precision in comparison to other prevalent methods. Before epigenetic treatments, chemotherapy was one of the most widely applied cancer treatments. Its main mechanism involves damaging the genetic material leading to either unsuccessful splitting or incomplete replication, thereby killing actively dividing cells. Thus, it may severely affect tissues with actively dividing cells, including hair, bone marrow, and epithelial cells during the treatment. Epigenetic treatments, on the other hand, target cancer biomarkers such as the GSTP1 gene which is specific to cancerous cells, thereby avoiding targeting other civilian cells which leads to side effects. Although many first and second generators epigenetic therapies in the last century targeted the epigenome globally which severely reduced the specificity of treatments as the drugs would often have wide impacts on many genes and lead to off-target effects, recent studies were able to integrate the dCas protein from the CRISPR-Cas9 technology as a novel drug delivering pathway. This was first proposed by Gilbert et al. in 2013 when they implemented non-coding guide RNAs to help the binding of deactivated Cas protein with the target promotors or repressors corresponding to the guide RNA sequence (30). Furthermore, epigenetic treatments can increase the effectiveness of other treatments by their synergistic effects in increasing the sensitivity of cancerous cells to certain treatments such as chemo and radiotherapy. For instance, androgen deprivation and androgen-receptor-targeting therapies are two gold-standard treatments for metastatic prostate cancer. However, acquired resistance to these treatments is a crucial challenge. In a 2022 review by Bagheri et al., researchers stressed that combinatorial therapy by epigenetic treatments that decrease protein kinase expression is a promising approach for metastatic PC treatment to decrease the tissue’s resistance to existing therapies. Later in a recent 2023 study, Murphy et al. applied anti-PD1 and anti-CTLA4 antibodies synergistically with vorinostat, a HADC inhibitor to reduce the cancerous tissue’s resistance for immune checkpoint blockade therapy, a common treatment for advanced prostate cancer (31). Despite its known advantages and potential, there are many problems and limitations due to the novelty of epigenetic treatments, including off-target effects, lack of biomarkers, resistance and the lack of valid trials. For many first and second-generation epigenetic therapies in the last century, treatments such as medicines that serve as activators or inhibitors often execute their functions globally, generating unintended changes on other gene locations, instead of specific loci. To be more specific, a DNA methyltransferase intended to limit the expression of an oncogene may alter some promoter sequences of a tumour suppressor gene adjacent to the target locus. This, unfortunately, causes a severe effect which would deteriorate the situation. Even as they avoided altering some important regulatory sequences in the cell cycle, they are still likely to interfere with the normal growth and function of the cell if not guided by a probe. Meanwhile, achieving high specificity for the targeted genes remains a great challenge, and there has been intense research ongoing focusing on understanding the mechanisms underlying off-target effects to decrease their off-target effects. Since the human prostate is a major endocrine gland that secretes androgen and semen in men, prostate cancers are often treated with hormonal therapies. During the first few years of clinical trials and applications, the treatment seems to work effectively. However, scientists found that resistance eventually developed in cancerous cells, leading to castration-resistant prostate cancer (CRPC). MicroRNAs (miRNAs) are a group of tiny RNA molecules that do not code for proteins. They control gene expression by either preventing the translation of target messenger RNAs (mRNAs) into proteins or by promoting the degradation of these target mRNAs (32). They are found to be dysregulated in cancerous cells resistant to bicalutamide, a common hormonal therapy drug (33). Normally, miRNAs act as transcriptional regulators by attaching to specific sequences in the 3’-untranslated region (3’-UTR) of target mRNAs (34). When miRNAs are not functioning correctly, it can disrupt various cellular and biological processes. This disruption can play a role in the development and advancement of human cancers by affecting different aspects of tumour biology, such as cell proliferation (35). Although researchers have studied many potential biomarkers in human prostate cancer, the mechanism of the interactions between the gene sequences in cancer cells is still undetermined. For instance, there is substantial evidence supporting the potential of DNA methylation detection as a valuable tumour biomarker. However, in the context of prostate cancer, only the GSTP1 gene demonstrates the necessary specificity and sensitivity for further evaluation as a tumour marker in body fluids. Even if new targets and biomarkers are proposed, there are not sufficient trials and validation for efficacy and precision due to the lack of research and some ethical issues, which is a major disadvantage for epigenetic treatments (26). Conclusion Some successes of this research are that I successfully explained the mechanism and logic of the approach, integrated recent findings in a cutting-edge area, included practical applications of known epi-drugs, and compared the effectiveness of epigenetic treatments with alternatives. To be more specific, I gathered clinical trial data for standard chemotherapy as a comparison to epigenetic treatments. Since I am not an expert in the field, the resource gathering cost me a lot of time. However, the limited clinical trials are still able to provide crucial and positive insights into the effectiveness of the treatment in comparison to chemotherapy. There were indeed some slight regrets to this research. To begin with, no first-hand resources and data are generated during my research period. This from one perspective limited the impact of this research essay. In addition, I underestimated the content of my field of research so I planned a bit over the word limit, so I did not introduce all prevalent treatments and drugs responsible. Finally, since epigenetic treatment for cancer is still a novel research field with only a few clinical trials carried out in the last decade, the impact of the trials was limited and the results were often incomprehensive to distinguish whether epigenetic treatments are more effective than chemotherapy. In a nutshell, the thesis of epigenetic treatments is derived mainly from the reversibility of epigenetic modifications and their aberrations detected in prostate cancer tissues. Naturally, epigenetic modifications are written in the chromosome by enzymes such as DNMTs and HDACs. Current epigenetic drugs mainly serve as either analogs or inhibitors for those enzymes to alter the epigenome. In this research essay, I summarised several aberrations observed in prostate cancer cells and explained some of the most often used first and second-generation drugs as well as their interactions with the transcriptional landscape and chromatin structure of our genes. Due to the novel research field, there remain some drawbacks of treatment due to our deficiency of knowledge in the underlying interactions between some enzymes, inhibitors and the epigenome. As one of the most commonly discussed and studied areas in molecular biology, epigenetics and their mechanism of interaction with the genome remained unclear for scientists. We still have a lot to figure out, such as the mechanism behind selective methylation, and the coexistence of hypermethylation and hypomethylation in prostate cancer cells before we can apply epigenetic drugs more efficiently. Although results from small clinical trials in the last decade remain fluctuating, some have already provided promising results that, in some circumstances, outweigh chemotherapeutics. Moreover, ongoing clinical trials have been continuing to provide valuable insights to the field which is making this treatment a feasible and viable approach to prostate cancer. 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