Anwesha Chatterjee, Amity University Kolkata
The novel Corona Virus (SARS-CoV-2) infection which is responsible for the COVID-19 pandemic is expecting an adverse effect on the progression of multiple cancers, i.e. prostate cancer, due to the transpiring cytokine storm associated with oncogenic signalling. Cancer progression can be prevented at an early stage by blocking SARS-COV-2 infection through potential therapies of host cell factors and their regulations. Host cell infections by SARS-COV-2 need priming of Viral spike S protein by serine protease TMPRSS2 which is encrypted by Androgen Response Gene and expressed in prostate cancer patients; the host cell also needed binding of the same protein to the ACE2 receptor.
Epidemiologically, the data showed increased severity and mortality in SARS-CoV-2 infected men, which suggested primary infection sites and other possible roles for Androgen in the transcriptional activation of ACE2 and TMPRSS2 receptors in mice tissue and human prostate and lung cell lines. Also, the endogenous interaction between the TMPRSS2 and ACE2 has been demonstrated in human cells, and ACE2 is substantiated as a TMPRSS2 substrate. Camostat ~ a TMPRSS2 inhibitor blocked the cleft of the SARS-COV-2 surface without obstructing ACE2 – TMPRSS2 interaction, in an overexpressed model of prostate and lung cells.
Altogether, the preclinical results showed a very strong ground of justification for clinical evaluation of androgen – deprivation therapy, TMPRSS2 inhibitors, and androgen receptor antagonist; or in amalgamation with antiviral drugs as clinically possible to prevent progression of Pneumonia and hyper inflammation response-driven to COVID-19 patients.
Also read: Covid Update: Moderna Vaccine on the Horizon!
Reference – https://www.biorxiv.org/content/10.1101/2020.10.16.342782v1
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