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Oncolytic herpes simplex virus and temozolomide synergistically inhibit breast cancer cell tumorigenesis in vitro and in vivo
The oncolytic herpes simplex virus (HSV) G47Δ can selectively eliminate glioblastoma cells via viral replication and temozolomide (TMZ) has been clinically used to treat glioblastoma. However, the combined effect of G47Δ and TMZ on cancer cells, particularly on breast cancer cells, remains largely u...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7751368/ https://www.ncbi.nlm.nih.gov/pubmed/33376532 http://dx.doi.org/10.3892/ol.2020.12360 |
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author | Fan, Jingjing Jiang, Hua Cheng, Lin Ma, Binlin Liu, Renbin |
author_facet | Fan, Jingjing Jiang, Hua Cheng, Lin Ma, Binlin Liu, Renbin |
author_sort | Fan, Jingjing |
collection | PubMed |
description | The oncolytic herpes simplex virus (HSV) G47Δ can selectively eliminate glioblastoma cells via viral replication and temozolomide (TMZ) has been clinically used to treat glioblastoma. However, the combined effect of G47Δ and TMZ on cancer cells, particularly on breast cancer cells, remains largely unknown. The objective of the present study was to investigate the role and underlying mechanism of G47Δ and TMZ, in combination, in breast cancer cell tumorigenesis. The human breast cancer cell lines SK-BR-3 and MDA-MB-468 were treated with G47Δ and TMZ individually or in combination. Cell viability, flow cytometry, reverse transcription quantitative-PCR and western blotting were performed to investigate the synergy between G47Δ and TMZ in regulating breast cancer cell behavior in vitro. The role of G47Δ and TMZ in suppressing tumorigenesis in vivo was investigated in a xenograft mouse model. G47Δ and TMZ served a synergistic role resulting in decreased breast cancer cell viability, induction of cell cycle arrest, promotion of tumor cell apoptosis and enhancement of DNA damage response in vitro. The combined administration of G47Δ and TMZ also effectively suppressed breast cancer cell-derived tumor growth in vivo, compared with the administration of G47Δ or TMZ alone. Synergy between G47Δ and TMZ was at least partially mediated via TMZ-induced acceleration of G47Δ replication, and such a synergy in breast cancer cells in vitro and in vivo provides novel insight into the future development of a therapeutic strategy against breast cancer. |
format | Online Article Text |
id | pubmed-7751368 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-77513682020-12-28 Oncolytic herpes simplex virus and temozolomide synergistically inhibit breast cancer cell tumorigenesis in vitro and in vivo Fan, Jingjing Jiang, Hua Cheng, Lin Ma, Binlin Liu, Renbin Oncol Lett Articles The oncolytic herpes simplex virus (HSV) G47Δ can selectively eliminate glioblastoma cells via viral replication and temozolomide (TMZ) has been clinically used to treat glioblastoma. However, the combined effect of G47Δ and TMZ on cancer cells, particularly on breast cancer cells, remains largely unknown. The objective of the present study was to investigate the role and underlying mechanism of G47Δ and TMZ, in combination, in breast cancer cell tumorigenesis. The human breast cancer cell lines SK-BR-3 and MDA-MB-468 were treated with G47Δ and TMZ individually or in combination. Cell viability, flow cytometry, reverse transcription quantitative-PCR and western blotting were performed to investigate the synergy between G47Δ and TMZ in regulating breast cancer cell behavior in vitro. The role of G47Δ and TMZ in suppressing tumorigenesis in vivo was investigated in a xenograft mouse model. G47Δ and TMZ served a synergistic role resulting in decreased breast cancer cell viability, induction of cell cycle arrest, promotion of tumor cell apoptosis and enhancement of DNA damage response in vitro. The combined administration of G47Δ and TMZ also effectively suppressed breast cancer cell-derived tumor growth in vivo, compared with the administration of G47Δ or TMZ alone. Synergy between G47Δ and TMZ was at least partially mediated via TMZ-induced acceleration of G47Δ replication, and such a synergy in breast cancer cells in vitro and in vivo provides novel insight into the future development of a therapeutic strategy against breast cancer. D.A. Spandidos 2021-02 2020-12-08 /pmc/articles/PMC7751368/ /pubmed/33376532 http://dx.doi.org/10.3892/ol.2020.12360 Text en Copyright: © Fan et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Fan, Jingjing Jiang, Hua Cheng, Lin Ma, Binlin Liu, Renbin Oncolytic herpes simplex virus and temozolomide synergistically inhibit breast cancer cell tumorigenesis in vitro and in vivo |
title | Oncolytic herpes simplex virus and temozolomide synergistically inhibit breast cancer cell tumorigenesis in vitro and in vivo |
title_full | Oncolytic herpes simplex virus and temozolomide synergistically inhibit breast cancer cell tumorigenesis in vitro and in vivo |
title_fullStr | Oncolytic herpes simplex virus and temozolomide synergistically inhibit breast cancer cell tumorigenesis in vitro and in vivo |
title_full_unstemmed | Oncolytic herpes simplex virus and temozolomide synergistically inhibit breast cancer cell tumorigenesis in vitro and in vivo |
title_short | Oncolytic herpes simplex virus and temozolomide synergistically inhibit breast cancer cell tumorigenesis in vitro and in vivo |
title_sort | oncolytic herpes simplex virus and temozolomide synergistically inhibit breast cancer cell tumorigenesis in vitro and in vivo |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7751368/ https://www.ncbi.nlm.nih.gov/pubmed/33376532 http://dx.doi.org/10.3892/ol.2020.12360 |
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