In vitro analysis suggests that SARS-CoV-2 infection differentially modulates cancer-like phenotypes - Differentially modulates cancer-like phenotypes

Sep 21, 2026

In vitro experiments evaluate how SARS-CoV-2 infection alters cancer-like traits and cytokine expression in prostate and colorectal cancer cells. Prostate (22RV1) and colorectal (DLD-1) lines expressing ACE2 are exposed to spike pseudovirus and live SARS-CoV-2. Researchers quantify phenotypic changes, cancer-marker gene expression (including Ki-67, BCL-2, VIM, MMP9, VEGF), and proinflammatory cytokines using MTT, wound healing assays, and RT-qPCR. Results indicate cell-type-specific effects on pathways governing growth, apoptosis, and migration.

LanguageEnglish

CategoryResearch & Report

FormatPDF

Pages11

Reading Time28 min

AccessFree to download

Abstract

Experimental design

Measured phenotypes and markers

Findings and implications

[www. nature.com/scientificreports](www. nature.com/scientificreports) OPEN In vitro analysis suggests that SARS-CoV-2 infection differentially modulates cancer-like phenotypesand cytokine expression in colorectal and prostate cancer cells Alberta Serwaa1,2, Fatima Oyawoye1, Irene Amoakoh Owusu1, Daniel Dosoo1, Aaron Adom Manu1,2, Augustine Kojo Sobo1,2, Kwadwo Fosu1,2, Charles Ochieng Olwal1,2, Peter Kojo Quashie1,3􀀍 & Anastasia Rosebud Aikins1,2􀀍 The coronavirus disease 2019 (COVID-19) reportedly exacerbates cancer outcomes. However, how COVID-19 influences cancer prognosis and development remains poorly understood. Here, we investigated the effect of Severe Acute Respiratory Syndrome CoronaVirus 2 (SARS-CoV-2), theetiological agent ofCOVID-19, on cellular cancer phenotypes the expression of cancer-related markers, and various proinflammatory cytokines. We infected prostate (22RV1) and colorectal (DLD-1) cancer cell lines, which express angiotensin-converting enzyme 2 (ACE2), with spike pseudovirus (sPV) and laboratory stocks of live SARS-CoV-2 viruses. After infection, we quantified changes in the cellular cancer phenotypes, the gene expression levels of some cancer markers, including Ki-67, BCL-2, VIM, MMP9, and VEGF, and proinflammatory cytokines. Phenotypic analysis was performed using MTT and wound healing assays, whereas gene expression analysis was carried out using real-time quantitative PCR (RT-qPCR). We show that SARS-CoV-2 infection impacts several key cellular pathways involved in cell growth, apoptosis, and migration, in prostate and colorectal cancer cells. Our results suggest that SARS-CoV-2 infection does influence various cancer cellular phenotypes and expression of molecular cancer markers and proinflammatory cytokines, albeit in a cell-type-specific manner. Our findings hint at the need for further studies and could have implications for evaluating the impact of other viruses on cancer progression. Keywords SARS-CoV-2, Cancer, COVID-19, Spike pseudovirus, Cytokine expression Cancer is among the leading causes of death worldwide1. While cancer development is multifaceted2,3, the complex mechanisms underlying the development of various cancers remain unresolved. Infectious agents, particularly viruses, have been associated with the development of various cancers. Currently, the seven viruses (oncogenic viruses) that have been associated with various cancers include Human papillomavirus (HPV), Epstein-Barr virus (EBV), Kaposi’s sarcoma-associated herpesvirus (KSHV), Human T-lymphotropic virus 1 (HTLV-1), Hepatitis B virus, Hepatitis C virus and Merkel cell polyomavirus4. One key mechanism by which oncogenic viruses cause cancer is by inducing the production of immunosuppressive cytokines in cells5 and remodeling the host molecular landscapes, enabling viruses to escape immune clearance, and causing uncontrolled cell proliferation. In 2019, the Coronavirus disease 2019 (COVID-19), caused by Severe Acute Respiratory Syndrome Corona Virus 2 (SARS-CoV-2), emerged and infected millions of individuals across the globe. SARS-CoV-2 can infect epithelial and endothelial cells of multiple organs including the lungs, kidneys, intestines, colon, brain, trachea, pancreas, testes, prostate, and blood vessels6,7. During infection, SARS-CoV-2 interacts and binds to host cells that express Angiotensin-converting Enzyme 2 (ACE2), the main entry receptor8. The observed presence of ACE2 on many cancer cells9–12 has stimulated 1West African Centre for Cell Biology of Infectious Pathogens (WACCBIP), College of Basic and Applied Sciences, University of Ghana, Accra, Ghana. 2Biochemistry, Cell, and Molecular Biology, College of Basic and Applied Sciences, University of Ghana, Accra, Ghana. 3Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK. 􀀍 email: [pquashie@ug.edu.gh](pquashie@ug.edu.gh); [araikins@ug.edu.gh](araikins@ug.edu.gh) [www. nature.com/scientificreports/](www. nature.com/scientificreport

FAQs

What experimental models were used to study SARS-CoV-2 effects on cancer phenotypes?

The study used prostate (22RV1) and colorectal (DLD-1) cancer cell lines that express ACE2, infected with spike pseudovirus and live SARS-CoV-2.

Which assays and molecular methods were used to quantify changes after infection?

Phenotypic changes were assessed with MTT and wound healing assays, while gene expression of cancer markers and related molecules was measured using RT-qPCR.

How did SARS-CoV-2 infection affect cancer-related pathways and cytokine expression?

SARS-CoV-2 influenced pathways involved in cell growth, apoptosis, and migration, and altered the expression of molecular cancer markers and proinflammatory cytokines in a cell-type-specific manner.

Sep 21, 2026

Uploaded by River Wang