Cancer Genetics and Epigenetics, 2025, Vol.13, No.2, 77-89 http://medscipublisher.com/index.php/cge 81 deacetylation of histones and non-histones, making the genes that originally inhibit tumors unable to function, while the genes that promote tumor growth are activated (Weichert et al., 2008; Li et al., 2020). For instance, the expression levels of HDAC1, HDAC2 and HDAC3 are relatively high in patients with prostate cancer. Among them, the high expression of HDAC2 is associated with the shortened recurrence time of PSA after prostate cancer surgery (Weichert et al., 2008). The overexpression of HDACs can cause tumor cells to proliferate more rapidly and differentiate abnormally, indicating that HDACs has a significant impact on exacerbating the malignancy of prostate cancer (Weichert et al., 2008; Hayashi et al., 2010). Figure 2 The role of HDAC and HDAC inhibitors (HDACi) in transcription regulation and the function of acetylation in chromatin structure and gene expression (Adapted from Li et al., 2020) Image caption: A: This illustrates the role of histone deacetylases (HDACs) and HDAC inhibitors (HDACi) in transcription regulation; HDACs interact with other epigenetic modification factors (such as methyltransferases and demethylases) to regulate chromatin structure and gene expression; Acetylation modifications promote gene expression by altering chromatin openness; B: The model shows the regulatory mechanism of HDAC and HDACi on the expression of oncogenes (such as Myc, AKT) and tumor suppressor genes (such as p53, p21); HDACi activate tumor suppressor genes and inhibit oncogene expression by disrupting HDAC activity, thereby affecting cell proliferation and apoptosis (Adapted from Li et al., 2020) 4.3 Therapeutic potential of HDAC inhibitors HDAC inhibitors (HDACi) have brought new hope for the treatment of prostate cancer. This type of drug inhibits the deacetylation function of HDACs, increases acetylated histones and non-histones, reactivates those originally "silent" genes, thereby preventing cancer cell division, inducing cancer cell death, and also inhibiting tumor angiogenesis (Glaser et al., 2003; Gui et al., 2004; Li et al., 2020). Methylene aniline hydroxamic acid (SAHA) is
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