The double-edged sword: How SARS-CoV-2 might fuel lung cancer: Investigating the potential oncogenic mechanisms of the novel coronavirus in lung carcinogenesis

The COVID-19 pandemic, caused by SARS-CoV-2, has had far-reaching consequences beyond acute respiratory illness, with growing evidence suggesting potential long-term oncogenic effects. Lung cancer, a leading cause of cancer-related mortality, may intersect with COVID-19 through shared molecular pathways and altered disease dynamics. SARS-CoV-2 can exacerbate outcomes in existing cancer patients and potentially contribute to de novo lung carcinogenesis or accelerate progression via chronic inflammation, oxidative stress, immune dysregulation, cellular senescence, cell cycle disruption, metabolic reprogramming, and autophagy impairment. It has been proven that although the SARS virus is not capable of integrating into the host genome, it uses the mechanisms of other human oncoviruses to cause lung cancer. Post-COVID-19 pulmonary fibrosis, observed in up to one-third of severe cases, may act as a tumor precursor bridge through sustained tissue remodeling, extracellular matrix stiffness, and hypoxia-induced epithelial-mesenchymal transition. Epidemiological studies indicate increased cancer-related mortality, metastatic reactivation of dormant cancer cells, and diagnostic delays, shifting presentations toward advanced stages during the pandemic. Synergistic risk factors, including smoking, air pollution, occupational exposures, and genetic predispositions, may further amplify oncogenic potential. The convergence of viral, environmental, and host factors creates a critical need for vigilant surveillance, biomarker development, and preventive strategies. This study aims to synthesize current epidemiological evidence, elucidate the molecular and cellular mechanisms by which SARS-CoV-2 may influence lung carcinogenesis, and highlight clinical implications to guide future research, screening, and therapeutic interventions.