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Research Article
Involvement of Bradykinin and Folate receptor in calming the SARS-COV2 cytokine storm: Lessons learnt from lung cancer
Ellora Sen
National Brain Research Centre
Corresponding Author
ORCiD: https://orcid.org/0000-0001-6842-7850
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Severe acute respiratory syndrome coronavirus (SARS-CoV2) is a highly pathogenic respiratory virus that causes morbidity and mortality in humans. The lungs are the major pathological target of SARS-CoV infection. The pathological derangements, aberrant signalling and dysregulated inflammation characteristics of lung cancer have marked similarities with the clinical manifestation of SARS-COV2 infection. As heightened inflammatory response is a key feature of both SARS-CoV infection and lung cancer and given the intriguing commonalities between the two, we analysed the RNA sequence dataset from lung cancer patients to get a better understanding of the critical regulators of inflammation in SAR-COV2.
Methods: The Cancer Genome Atlas (TCGA) data sets of lung cancer were analyzed for correlations between ACE2, Bradykinin, and other genes associated with inflammatory responses.
Results: TCGA dataset analysis indicated an inverse correlation between ACE2 and Bradykinin Receptor 1 (BDKRB1), IL-6 and IFNg in lung adenocarcinoma. A positive correlation between EGF, FOLR1, MAOA, NOSTRIN, MARC2, PHKD1, and ACE2 was noted
Summary: Our analysis has identified a common (i) ACE2- BDKRB1-inflammatory network and (ii) FOLR1-Nitric oxide cross-talk in lung cancer and SARS-CoV2. Better understanding of the convergences between critical players in these networks would enable efficient repurposing of approved lung cancer therapeutics for COVID-19 infection.
Keywords
COVID-19, ACE2, BDKRB1, Nitric Oxide, Folate, Inflammation
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This is a preprint. It has not completed peer review.
Research Article
Involvement of Bradykinin and Folate receptor in calming the SARS-COV2 cytokine storm: Lessons learnt from lung cancer
Ellora Sen
National Brain Research Centre
Corresponding Author
ORCiD: https://orcid.org/0000-0001-6842-7850
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 22 Apr, 2020
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Severe acute respiratory syndrome coronavirus (SARS-CoV2) is a highly pathogenic respiratory virus that causes morbidity and mortality in humans. The lungs are the major pathological target of SARS-CoV infection. The pathological derangements, aberrant signalling and dysregulated inflammation characteristics of lung cancer have marked similarities with the clinical manifestation of SARS-COV2 infection. As heightened inflammatory response is a key feature of both SARS-CoV infection and lung cancer and given the intriguing commonalities between the two, we analysed the RNA sequence dataset from lung cancer patients to get a better understanding of the critical regulators of inflammation in SAR-COV2.
Methods: The Cancer Genome Atlas (TCGA) data sets of lung cancer were analyzed for correlations between ACE2, Bradykinin, and other genes associated with inflammatory responses.
Results: TCGA dataset analysis indicated an inverse correlation between ACE2 and Bradykinin Receptor 1 (BDKRB1), IL-6 and IFNg in lung adenocarcinoma. A positive correlation between EGF, FOLR1, MAOA, NOSTRIN, MARC2, PHKD1, and ACE2 was noted
Summary: Our analysis has identified a common (i) ACE2- BDKRB1-inflammatory network and (ii) FOLR1-Nitric oxide cross-talk in lung cancer and SARS-CoV2. Better understanding of the convergences between critical players in these networks would enable efficient repurposing of approved lung cancer therapeutics for COVID-19 infection.
Figure 1
Figure 2
Figure 3