In addition, single-cell sequencing data from 27,414 cells from six CRC patients in the National Center for Biotechnology Information Gene Expression Omnibus (GEO) database (GSE144735), we found that ACE2, TMPRSS2, CTSL, and CTSB were primarily expressed in stromal and epithelial cells of CRC tissue (Figure 1B, C). SARS-CoV-2 usually enters cells through the endosomal pathway, but in the absence of TMPRSS2, it enters by cathepsin L (CTSL) and cathepsin B (CTSB) proteolysis and activation of S protein.ĭata on mRNA expression in colorectal cancer tissue in the Cancer Genome Atlas ( ) and the Genotype-Tissue Expression project ( ) databases, we found that the expression of ACE2 and TMPRSS2 was higher in CRC than in healthy tissue (Figure 1A). If transmembrane serine protease 2 (TMPRSS2) is present, it promotes the cleavage and activation of S proteins by host cells. SARS-COV-2 RECOGNITION PROTEINS ARE HIGHLY EXPRESSED IN THE TUMOR TISSUES OF CRC PATIENTSĪfter SARS-CoV-2 infection, viral envelope spike proteins bind to ACE2 and promote cellular recognition of the virus. We used CRC as an example to elucidate the effect of SARS-CoV-2 on the cancer immune microenvironment, especially the impact on monocytes, with the goal of finding treatments to delay the progression of COVID-19. Studies have also shown that COVID-19 patients with CRC are more likely to have clinical characteristics with a poor COVID-19 prognosis than matched patients with COVID-19 but without cancer. The results of meta-analysis and bioinformatics analysis have shown that colorectal cancer (CRC) patients are more susceptible to SARS-CoV-2 than cancer patients with other tumors. By comparing the differences in proteomics and metabolomics of severe and nonsevere COVID-19 cases with healthy controls, it was found that the severe cases were associated with abnormal macrophage regulation.

The leading cause of COVID-19 aggravation is multiorgan dysfunction caused by the cytokine release syndrome (CRS). Therefore, revealing the effects of COVID-19 infection on the human body may provide new ideas for preventing the deterioration of COVID-19 patients. However, the mechanism of the exacerbation of COVID-19 is not clear. Compared with patients without cancer, those with cancer have a 3.56-fold increased risk of severe disease following COVID-19 infection. Studies have shown that cancer patients not only have a 2.31 times higher risk of infection with SARS-CoV-2 than the general population but also have a higher risk of developing severe COVID-19. Clarifying the expression of those proteins unique to various human pathologies may be helpful in identifying susceptible populations. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) enters cells by recognizing angiotensin I converting enzyme 2 (ACE2), transmembrane serine protease 2 (TMPRSS2), and other proteases, such as cathepsin B (CTSB) and cathepsin L (CTSL), in the host cell. In particular, cancer patients are more vulnerable to virus infection because of their suppressed immune microenvironment. As a public health emergency of international concern, there are nearly 150 million coronavirus disease 2019 (COVID-19) cases worldwide.

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