Cardiovascular-oncogenic gene crosstalk in breast cancer: Survival, prognosis and therapeutic strategies

Figure 1 Effects of cardiovascular-oncogenic genes on the expression of associated cytokines in breast cancer and cardiovascular disorders. The figure illustrates the regulatory network linking cardiovascular-oncogenic genes (Janus kinase 2, titin, Tet methylcytosine dioxygenase 2, G protein-coupled receptor kinase 4, AMP-activated protein kinase, peroxisome proliferator-activated receptor gamma, and wingless-related integration site/β-catenin) with key inflammatory and pro-fibrotic cytokines [tumor necrosis factor-α, interleukin-6 (IL-6), IL-1β, and transforming growth factor-β]. Solid arrows indicate positive regulatory interactions or activation, whereas blunt-ended lines indicate inhibitory interactions. Elevated expression of tumor necrosis factor-α, IL-6, and IL-1β contributes to a pro-inflammatory tumor microenvironment and vascular dysfunction, while transforming growth factor-β promotes epithelial-mesenchymal transition, tissue fibrosis, immune suppression, and extracellular matrix deposition. Collectively, these molecular interactions drive adverse disease outcomes, including breast cancer progression (tumor growth, invasion and metastasis, therapy resistance, and poor prognosis) and cardiovascular disease (atherosclerosis, myocardial infarction, hypertension, heart failure, and arrhythmias). JAK2: Janus kinase 2; TTN: Titin; TET2: Tet methylcytosine dioxygenase 2; GRK4: G protein-coupled receptor kinase 4; AMPK: AMP-activated protein kinase; PPAR-γ: Peroxisome proliferator-activated receptor gamma; Wnt: Wingless-related integration site; TNF-α: Tumor necrosis factor alpha; IL-6: Interleukin-6; IL-1β: Interleukin-1β; TGF-β: Transforming growth factor-β.