Abstract:
Epigenetics' role in non-small cell lung cancer (NSCLC) and coronary artery disease (CAD) is currently emerging as a crucial player at several levels, ranging from pathophysiology to treatments. We aim to determine the combination of certain regular epigenetic controls that determine the pattern of methylation/demethylation or acetylation/deacetylation on different gene promoters linked to their pathogenesis. Certain genes, such as VEGFA, AIMP1, and so on, exhibit either up- or down-regulation in a pattern that is consistent with the involvement of many DNA damage (e.g., H2A.X) and repair factors (e.g., BRCA1, RAD51, ERCC1, XPF), transcription-coupled DNA repair factor, and replication proteins. Furthermore, aberrant histone methylation was discovered to be associated with BRCA1 complex in patients with CAD and NSCLC, among other epigenetic alterations. Although they altered the R-loop formation, which is susceptible to DNA damage, epigenetic therapies such the CRISPR/Cas9 mediated elimination or overexpression of a specific gene (BRCA1) showed encouraging alterations in sick circumstances. Together, invasive ductal carcinoma (IDC) and coronary artery disease (CAD) continue to be the leading causes of death in women each year. These conditions are caused by intricate signaling pathways and share a number of risk factors. Therefore, it's critical to identify the same epigenetic changes that may be causing the disease to proceed from CAD to IDC. Numerous epigenetic regulators, such as VEGFA and AIMP1, have been found. These regulators primarily function in inflammatory pathways in both disease states and changes in the epitranscriptome, such as aberrant m6A RNA methylation, in CD4+T helper cells in both CAD and IDC. Through the regulation of m6A RNA methylation and the tumor suppressor gene P53, CRISPR-Cas9 driven knockout/overexpression of a specific gene (BRCA1) presents a possible therapeutic method in sick circumstances. Furthermore, it had an impact on the establishment of the R-loop, which is susceptible to DNA damage. BRCA1 can also cause CTL-mediated cytotoxicity in breast cancer cells. Therefore, by comprehending the changes and interactions of epigenetic pathways, fresh treatment techniques to prevent the potential transmission of disease to disease can be developed. The involvement of common epigenetic mechanisms, as well as the interactions and modifications that our study discovered, will play a crucial role in helping to comprehend the upcoming development of innovative epigenetic therapeutics.
Audience Take Away Notes:
- The audience will discover that patients with CAD have an increased risk of breast and lung cancer.
- The researcher will be able to create several immunotherapeutic approaches for tumors with the aid of the mechanistic relationship between CAD and lung and breast cancer.
- Our work will facilitate future research by other scientists investigating the distinct epigenetic and epitranscriptomic mechanisms involved in these three interrelated disorders.
- Our results underscore the need for epigenetic and epitranscriptomic therapeutics for the disabling forms of CAD, lung cancer, and breast cancer, and they add to the body of information concerning therapeutic approaches that use inflammatory cytokines as a prognostic marker.
- Our research will undoubtedly advance in identifying multiple connections between CAD and lung cancer and breast cancer in order to create novel immunotherapeutic approaches to treat those illnesses.
