Cancer Genetics and Epigenetics 2024, Vol.12, No.3, 115-124 http://medscipublisher.com/index.php/cge 117 progression. Understanding these pathways and interactions is crucial for developing targeted therapies for gastric cancer. Figure 1 Biological pathways of gastric cancer mechanisms (Adopted from Lee et al., 2022) Image caption: THBS3, EFNA1, and PRKAA1 are involved in PI3K-Alt-mTOR-signaling pathway which is the key pathway associated with gastric cancer. MUC1 interacted with ICAM-1, CD11b, EGFR, Src, and CTNNB1 in PPI network is a regulator of the PI3K-Alt-mTOR-signaling pathway. PPI, protein-protein interaction (Adopted from Lee et al., 2022) Furthermore, a meta-analysis of GWAS and prospective cohort studies demonstrated that genetic risk models, such as polygenic risk scores, can effectively stratify individuals based on their risk of developing GC (Tuan et al., 2021). The study of Jin et al. (2020) also emphasized the potential of lifestyle modifications to mitigate the genetic risk of GC, suggesting that individuals with a high genetic risk could substantially reduce their risk by adopting a healthy lifestyle. In summary, the genetic landscape of GC is shaped by a complex interplay of oncogenes, tumor suppressor genes, chromosomal aberrations, and genetic variants identified through GWAS. Understanding these genetic insights is crucial for developing targeted therapies and improving the prognosis of GC patients. 3 Epigenetic Mechanisms in Gastric Cancer 3.1 DNA methylation DNA methylation is a critical epigenetic modification that involves the addition of a methyl group to the cytosine residues in CpG dinucleotides, leading to gene silencing. In gastric cancer, aberrant DNA methylation patterns are frequently observed and are associated with the inactivation of tumor suppressor genes and the activation of oncogenes (Biswas and Rao, 2017). This epigenetic alteration is considered a hallmark of gastric cancer and plays a significant role in its pathogenesis (Ebrahimi et al., 2020). Studies have shown that hypermethylation of promoter regions in tumor suppressor genes can lead to their silencing, contributing to cancer development and progression (Qu et al., 2013). Additionally, global hypomethylation can activate oncogenes, further promoting malignancy (Puneet et al., 2018). The potential of DNA methylation as a
RkJQdWJsaXNoZXIy MjQ4ODYzNQ==