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SARS-CoV-2 M Protein Facilitates Malignant Transformation of Breast Cancer Cells

Coronavirus disease 2019 (COVID-19) has spread faster due to the emergence of SARS-CoV-2 variants, which carry an increased risk of infecting patients with comorbidities, such as breast cancer. However, there are still few reports on the effects of SARS-CoV-2 infection on the progression of breast c...

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Autores principales: Nguyen, Hoai-Nga Thi, Kawahara, Marie, Vuong, Cat-Khanh, Fukushige, Mizuho, Yamashita, Toshiharu, Ohneda, Osamu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9209714/
https://www.ncbi.nlm.nih.gov/pubmed/35747796
http://dx.doi.org/10.3389/fonc.2022.923467
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author Nguyen, Hoai-Nga Thi
Kawahara, Marie
Vuong, Cat-Khanh
Fukushige, Mizuho
Yamashita, Toshiharu
Ohneda, Osamu
author_facet Nguyen, Hoai-Nga Thi
Kawahara, Marie
Vuong, Cat-Khanh
Fukushige, Mizuho
Yamashita, Toshiharu
Ohneda, Osamu
author_sort Nguyen, Hoai-Nga Thi
collection PubMed
description Coronavirus disease 2019 (COVID-19) has spread faster due to the emergence of SARS-CoV-2 variants, which carry an increased risk of infecting patients with comorbidities, such as breast cancer. However, there are still few reports on the effects of SARS-CoV-2 infection on the progression of breast cancer, as well as the factors and mechanisms involved. In the present study, we investigated the impact of SARS-CoV-2 proteins on breast cancer cells (BCC). The results suggested that SARS-CoV-2 M protein induced the mobility, proliferation, stemness and in vivo metastasis of a triple-negative breast cancer (TNBC) cell line, MDA-MB-231, which are involved in the upregulation of NFκB and STAT3 pathways. In addition, compared to MDA-MB-231 cells, the hormone-dependent breast cancer cell line MCF-7 showed a less response to M protein, with the protein showing no effects of promoting proliferation, stemness, and in vivo metastasis. Of note, coculture with M protein-treated MDA-MB-231 cells significantly induced the migration, proliferation, and stemness of MCF-7 cells, which are involved in the upregulation of genes related to EMT and inflammatory cytokines. Therefore, SARS-CoV-2 infection might promote the ability of aggressive BCC to induce the malignant phenotypes of the other non-aggressive BCC. Taken together, these findings suggested an increased risk of poor outcomes in TNBC patients with a history of SARS-CoV-2 infection, which required a long-term follow-up. In addition, the inhibition of NFκB and STAT3 signaling pathways is considered as a promising candidate for the treatment of worsen clinical outcomes in TNBC patients with COVID-19.
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spelling pubmed-92097142022-06-22 SARS-CoV-2 M Protein Facilitates Malignant Transformation of Breast Cancer Cells Nguyen, Hoai-Nga Thi Kawahara, Marie Vuong, Cat-Khanh Fukushige, Mizuho Yamashita, Toshiharu Ohneda, Osamu Front Oncol Oncology Coronavirus disease 2019 (COVID-19) has spread faster due to the emergence of SARS-CoV-2 variants, which carry an increased risk of infecting patients with comorbidities, such as breast cancer. However, there are still few reports on the effects of SARS-CoV-2 infection on the progression of breast cancer, as well as the factors and mechanisms involved. In the present study, we investigated the impact of SARS-CoV-2 proteins on breast cancer cells (BCC). The results suggested that SARS-CoV-2 M protein induced the mobility, proliferation, stemness and in vivo metastasis of a triple-negative breast cancer (TNBC) cell line, MDA-MB-231, which are involved in the upregulation of NFκB and STAT3 pathways. In addition, compared to MDA-MB-231 cells, the hormone-dependent breast cancer cell line MCF-7 showed a less response to M protein, with the protein showing no effects of promoting proliferation, stemness, and in vivo metastasis. Of note, coculture with M protein-treated MDA-MB-231 cells significantly induced the migration, proliferation, and stemness of MCF-7 cells, which are involved in the upregulation of genes related to EMT and inflammatory cytokines. Therefore, SARS-CoV-2 infection might promote the ability of aggressive BCC to induce the malignant phenotypes of the other non-aggressive BCC. Taken together, these findings suggested an increased risk of poor outcomes in TNBC patients with a history of SARS-CoV-2 infection, which required a long-term follow-up. In addition, the inhibition of NFκB and STAT3 signaling pathways is considered as a promising candidate for the treatment of worsen clinical outcomes in TNBC patients with COVID-19. Frontiers Media S.A. 2022-06-07 /pmc/articles/PMC9209714/ /pubmed/35747796 http://dx.doi.org/10.3389/fonc.2022.923467 Text en Copyright © 2022 Nguyen, Kawahara, Vuong, Fukushige, Yamashita and Ohneda https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Oncology
Nguyen, Hoai-Nga Thi
Kawahara, Marie
Vuong, Cat-Khanh
Fukushige, Mizuho
Yamashita, Toshiharu
Ohneda, Osamu
SARS-CoV-2 M Protein Facilitates Malignant Transformation of Breast Cancer Cells
title SARS-CoV-2 M Protein Facilitates Malignant Transformation of Breast Cancer Cells
title_full SARS-CoV-2 M Protein Facilitates Malignant Transformation of Breast Cancer Cells
title_fullStr SARS-CoV-2 M Protein Facilitates Malignant Transformation of Breast Cancer Cells
title_full_unstemmed SARS-CoV-2 M Protein Facilitates Malignant Transformation of Breast Cancer Cells
title_short SARS-CoV-2 M Protein Facilitates Malignant Transformation of Breast Cancer Cells
title_sort sars-cov-2 m protein facilitates malignant transformation of breast cancer cells
topic Oncology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9209714/
https://www.ncbi.nlm.nih.gov/pubmed/35747796
http://dx.doi.org/10.3389/fonc.2022.923467
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