Abstract
Cancer and viruses have a long history that has evolved over many decades. Much information about the interplay between viruses and cell proliferation and metabolism has come from the history of clinical cases of patients infected with virus-induced cancer. In addition, information from viruses used to treat some types of cancer is valuable. Now, since the global coronavirus pandemic erupted almost a year ago, the scientific community has invested countless time and resources to slow down the infection rate and diminish the number of casualties produced by this highly infectious pathogen. A large percentage of cancer cases diagnosed are strongly related to dysregulations of the tyrosine kinase receptor (TKR) family and its downstream signaling pathways. As such, many therapeutic agents have been developed to strategically target these structures in order to hinder certain mechanisms pertaining to the phenotypic characteristics of cancer cells such as division, invasion or metastatic potential. Interestingly, several authors have pointed out that a correlation between coronaviruses such as the SARS-CoV-1 and -2 or MERS viruses and dysregulations of signaling pathways activated by TKRs can be established. This information may help to accelerate the repurposing of clinically developed anti-TKR cancer drugs in COVID-19 management. Because the need for treatment is critical, drug repurposing may be an advantageous choice in the search for new and efficient therapeutic compounds. This approach would be advantageous from a financial point of view as well, given that the resources used for research and development would no longer be required and can be potentially redirected towards other key projects. This review aims to provide an overview of how SARS-CoV-2 interacts with different TKRs and their respective downstream signaling pathway and how several therapeutic agents targeted against these receptors can interfere with the viral infection. Additionally, this review aims to identify if SARS-CoV-2 can be repurposed to be a potential viral vector against different cancer types.
Highlights
Coronaviruses are RNA viruses that affect mammals, having an affinity for the respiratory apparatus in humans
This review aims to provide an overview of how SARS-CoV-2 interacts with different tyrosine kinase receptor (TKR) and their respective downstream signaling pathway and how several therapeutic agents targeted against these receptors can interfere with the viral infection
Another relation between SARS-CoV-2 and TKR activity in cancer might be established between the large number of proinflammatory cytokines and chemokines, which are largely responsible for acute respiratory distress syndrome and the tumor microenvironment, which has a strong impact on carcinogenesis; more explicitly, a link between the IL-6/JAK/STAT3 pathway and the plethora of proinflammatory molecules found in patients suffering from COVID-19
Summary
Coronaviruses are RNA viruses that affect mammals, having an affinity for the respiratory apparatus in humans. Cases with longer incubation periods, up to 24 days, have been reported [6] This long incubation period, through which the patients present no symptoms but are contagious, is considered one of the main reasons why SARS-CoV-2 has spread so fast around the world [5]. After this asymptomatic period, the symptoms that usually appear are the following: fever, fatigue, cough, headache, difficulty in breathing, hemoptysis, sputum production, sore throat and diarrhea [7,8]. Another way of explaining this discrepancy is that the EGFR downstream signaling kinetics could be dysregulated and not necessarily dependent on the strength of the signal itself [37]
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