This is a preprint. Preprints are preliminary reports that have not undergone peer review. They should not be considered conclusive, used to inform clinical practice, or referenced by the media as validated information.
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
Declarations:
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
Declarations:
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