World-class cancer researcher shows spike protein from SARS-Cov-2 virus blunts a vital pathway in tumor suppression.
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In March 2020, Wafik El-Deiry, a distinguished oncologist and professor at Brown University, embarked on a groundbreaking exploration in the early days of the pandemic. He pondered the possibility of the novel SARS-Cov-2 virus increasing an individual’s susceptibility to cancer. This was not an entirely novel concept but a less traveled path.
“We’ve long been aware of the link between certain viruses and cancer, such as Hepatitis B or C, Epstein Bar Virus, Human Papilloma Virus, and Kaposi's sarcoma herpesvirus,” elaborated El-Deiry. “So, I couldn't help but wonder if SARS-Cov-2, with its unique characteristics, could potentially pave the way for cancer in the future.”
As a world leader in cancer research, El-Deiry’s groundbreaking work has been centered around a cellular pathway that plays a pivotal role in cancer development, known as the p53 pathway.
p53 suppresses tumor growth, and any perturbation of this pathway can cause unregulated cell division, leading to cancer.
“Since the 1990s, my lab is well-known for identifying genes downstream of p53 that regulate its function,” said El-Deiry. “It’s the most commonly mutated gene in human cancers, and that’s why I’ve dedicated my life to studying p53.”
From his 2023 paper titled,
Key Statement:
As there is already a history of various viruses associated with human cancer including hepatitis viruses HBV/HCV, EBV, HPV, and potentially SV40, SARS-CoV-2 is a candidate that should be further investigated.
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and COVID-19 infection has led to worsened outcomes for patients with cancer. SARS-CoV-2 spike protein mediates host cell infection and cell-cell fusion that causes stabilization of tumor suppressor p53 protein. In-silico analysis previously suggested that SARS-CoV-2 spike interacts with p53 directly but this putative interaction has not been demonstrated in cells.
We examined the interaction between SARSCoV-2 spike, p53 and MDM2 (E3 ligase, which mediates p53 degradation) in cancer cells using an immunoprecipitation assay.
We observed that SARS-CoV-2 spike protein interrupts p53- MDM2 protein interaction but did not detect SARS-CoV-2 spike bound with p53 protein in the cancer cells.
We further observed that SARS-CoV-2 spike suppresses p53 transcriptional activity in cancer cells including after nutlin exposure of wild-type p53-, spike S2-expressing tumor cells and inhibits chemotherapy-induced p53 gene activation of p21(WAF1), TRAIL Death Receptor DR5 and MDM2.
The suppressive effect of SARS-CoV-2 spike on p53-dependent gene activation provides a potential molecular mechanism by which SARS-CoV-2 infection may impact tumorigenesis, tumor progression and chemotherapy sensitivity. In fact, cisplatin-treated tumor cells expressing spike S2 were found to have increased cell viability as compared to control cells. Further observations on g-H2AX expression in spike S2-expressing cells treated with cisplatin may indicate altered DNA damage sensing in the DNA damage response pathway.
The preliminary observations reported here warrant further studies to unravel the impact of SARSCoV-2 and its various encoded proteins including spike on pathways of tumorigenesis and response to cancer therapeutics
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