**4. Therapeutic potentials and limitations**

Epigenetic drugs are chemicals that alter DNA and chromatin structure, promoting the disruption of transcriptional and post-transcriptional modifications, primarily by regulating the enzymes required for their establishment and maintenance, and reactivating epigenetically silenced tumor-suppressor and DNA repair genes [161]. The development of treatment techniques incorporating epigenetic medicines, which focus on the cancer epigenome to generate pharmacological molecules that could restore a "normal" epigenetic landscape, is a developing field of drug discovery [161]. Epigenetic medicines target the enzymes that are required for the maintenance and establishment of epigenetic alterations, with the inhibition of DNMTs and HDACs being the most common technique [161]. The epigenetic alterations caused by these medications can regulate the temporal and spatial expression of genes [162], and they have ramifications for the regulation and dysregulation of physiological and pathological processes. Because epigenetic markings are tightly linked to the type of tumor and stage of disease, as well as individual genetic variation, such as in personalized medicine [163, 164], they have a lot of promise to give molecular biomarkers for diagnosis and treatment alternatives for cancer therapy [165].

The FDA has approved six new epigenetic medicines and multi-drug regimens for use in clinical cancer treatment. Some side effects will happen, so novel epigenetic therapeutic compounds are continually being tested in preclinical research, as well as clinical trials for the development and release of new medicines, for cytotoxicity, and pharmacological characteristics, and to better understand their mechanism of action. The majority of epigenetic medication studies are focused on cancer detection, therapy, and prognosis.

NcRNAs have shown new promise and insight as therapeutic targets for cancer treatment and preventing cancer metastasis in vivo preclinical models of metastatic illness. Research has shown that lncMAYA, MALAT1, and lncARSR have all been targeted for in vivo suppression using ASOs in mice models to alleviate the burden of metastatic disease [110, 166–168]. When targeting lncRNAs with ASO therapies, however, it will be vital to ensure minimal off-target effects [169, 170], which could offer additional challenges given the decreased quantity of lncRNA transcripts in vivo. ASOs disrupt target RNAs by premature transcriptional termination [171, 172], in addition to RNase H-mediated destruction of mature RNA, according to new findings, which should be taken into account when estimating the efficacy of ASO therapies. The biggest problem is the species conservatism in ncRNA, especially lncRNAs. Animal testing is also required before conducting clinical trials.
