Fig. 2

Schematic illustration depicting the shared mechanisms between SARS-CoV-2 and key hallmarks of cancer including sustained proliferative signaling, resisting cell death, genomic instability, dysregulated cellular metabolism and epigenetic reprogramming. The diagram highlights how SARS-CoV-2 interacts with critical oncogenic signaling molecules or pathways. Specific SARS-CoV-2 proteins involved in these processes are marked: NSP (Non-Structural Proteins), N (Nucleocapsid Protein), M (Membrane Protein) and S (Spike Protein). p53, Tumor Protein 53; pRB, Retinoblastoma Protein; RAAS, Renin–Angiotensin–Aldosterone System; E2F1, E2F Transcription Factor 1; SIRT5, Sirtuin 5; ANGII/AT1R, Angiotensin II/Angiotensin II Type 1 Receptor; MAPK/ERK1/2, Mitogen-Activated Protein Kinase/Extracellular Signal-Regulated Kinase 1/2; TGF-β, Transforming Growth Factor Beta; MUC1C, Mucin 1, Cell Surface Associated; MUC5AC, Mucin 5AC; TUB1AC, Tubulin Alpha; CREB, cAMP Response Element-Binding Protein; Eph receptor, Ephrin Receptor; RTK, Receptor Tyrosine Kinase; TGFR, Transforming Growth Factor Receptor; ATR, Ataxia Telangiectasia and Rad3-Related Protein; C-RAF, RAF Proto-Oncogene Serine/Threonine-Protein Kinase; HSP27, Heat Shock Protein 27; BAK, BCL2 Antagonist/Killer; MCL1, Myeloid Cell Leukemia 1; HLAC, Human Leukocyte Antigen C; HSPAIL, Heat Shock Protein A1-like; DNMT1, DNA Methyltransferase 1; ROS, Reactive Oxygen Species; NO, Nitric Oxide; HIF1-α, Hypoxia-Inducible Factor 1-Alpha. This image was created using BioRender software