Biological effects of COVID-19 on lung cancer: Can we drive our decisions

Abstract

COVID-19 infection caused by SARS-CoV-2 is considered catastrophic because it affects multiple organs, particularly those of the respiratory tract. Although the consequences of this infection are not fully clear, it causes damage to the lungs, the cardiovascular and nervous systems, and other organs, subsequently inducing organ failure. In particular, the effects of SARS-CoV-2-induced inflammation on cancer cells and the tumor microenvironment need to be investigated. COVID-19 may alter the tumor microenvironment, promoting cancer cell proliferation and dormant cancer cell (DCC) reawakening. DCCs reawakened upon infection with SARS-CoV-2 can populate the premetastatic niche in the lungs and other organs, leading to tumor dissemination. DCC reawakening and consequent neutrophil and monocyte/macrophage activation with an uncontrolled cascade of pro-inflammatory cytokines are the most severe clinical effects of COVID-19. Moreover, neutrophil extracellular traps have been demonstrated to activate the dissemination of premetastatic cells into the lungs. Further studies are warranted to better define the roles of COVID-19 in inflammation as well as in tumor development and tumor cell metastasis; the results of these studies will aid in the development of further targeted therapies, both for cancer prevention and the treatment of patients with COVID-19.

Keywords: COVID-19; genes; lung cancer; mutations; pandemic; virus.

Figure 1

Graphical illustration of the expression of the key proteins in lung cancer and COVID-19. ACE2 and PAI-1 are expressed at high levels in lung cancer and cause inflammation and neo-angiogenesis in COVID-19. TMPRSS2 helps SARS-COV-2 to enter the host cells, whereas CD147 and FURIN are associated with genomic susceptibility to COVID‐19 in patients with lung cancer.

Figure 2

Invasion with SARS-CoV-2. The ACE2 receptor is the channel through which the virus attaches to the cells via its S protein and enters the cell. A massive immune response through the amplification of NK and T cells is thereby triggered, leading to the production of a wide range of cytokines, such as interferon-γ, tumor necrosis factor, interleukin (IL)-1, IL-6, and IL-18, which are responsible for the cytokine storm.