B7-H3 suppresses doxorubicin-induced senescence-like growth arrest in colorectal cancer through the AKT/TM4SF1/SIRT1 pathway

Emerging evidence suggests that cellular senescence induced by chemotherapy has been recognized as a new weapon for cancer therapy. This study aimed to research novel functions of B7-H3 in cellular senescence induced by a low dose of doxorubicin (DOX) in colorectal cancer (CRC). Here, our results de...

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Autores principales: Wang, Ruoqin, Sun, Linqing, Xia, Suhua, Wu, Hongya, Ma, Yanchao, Zhan, Shenghua, Zhang, Guangbo, Zhang, Xueguang, Shi, Tongguo, Chen, Weichang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2021
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Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8102521/
https://www.ncbi.nlm.nih.gov/pubmed/33958586
http://dx.doi.org/10.1038/s41419-021-03736-2
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author Wang, Ruoqin
Sun, Linqing
Xia, Suhua
Wu, Hongya
Ma, Yanchao
Zhan, Shenghua
Zhang, Guangbo
Zhang, Xueguang
Shi, Tongguo
Chen, Weichang
author_facet Wang, Ruoqin
Sun, Linqing
Xia, Suhua
Wu, Hongya
Ma, Yanchao
Zhan, Shenghua
Zhang, Guangbo
Zhang, Xueguang
Shi, Tongguo
Chen, Weichang
author_sort Wang, Ruoqin
collection PubMed
description Emerging evidence suggests that cellular senescence induced by chemotherapy has been recognized as a new weapon for cancer therapy. This study aimed to research novel functions of B7-H3 in cellular senescence induced by a low dose of doxorubicin (DOX) in colorectal cancer (CRC). Here, our results demonstrated that B7-H3 knockdown promoted, while B7-H3 overexpression inhibited, DOX-induced cellular senescence. B7-H3 knockdown dramatically enhanced the growth arrest of CRC cells after low-dose DOX treatment, but B7-H3 overexpression had the opposite effect. By RNA-seq analysis and western blot, we showed that B7-H3 prevented cellular senescence and growth arrest through the AKT/TM4SF1/SIRT1 pathway. Blocking the AKT/TM4SF1/SIRT1 pathway dramatically reversed B7-H3-induced resistance to cellular senescence. More importantly, B7-H3 inhibited DOX-induced cellular senescence of CRC cells in vivo. Therefore, targeting B7-H3 or the B7-H3/AKT/TM4SF1/SIRT1 pathway might be a new strategy for promoting cellular senescence-like growth arrest during drug treatment in CRC.
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spelling pubmed-81025212021-05-10 B7-H3 suppresses doxorubicin-induced senescence-like growth arrest in colorectal cancer through the AKT/TM4SF1/SIRT1 pathway Wang, Ruoqin Sun, Linqing Xia, Suhua Wu, Hongya Ma, Yanchao Zhan, Shenghua Zhang, Guangbo Zhang, Xueguang Shi, Tongguo Chen, Weichang Cell Death Dis Article Emerging evidence suggests that cellular senescence induced by chemotherapy has been recognized as a new weapon for cancer therapy. This study aimed to research novel functions of B7-H3 in cellular senescence induced by a low dose of doxorubicin (DOX) in colorectal cancer (CRC). Here, our results demonstrated that B7-H3 knockdown promoted, while B7-H3 overexpression inhibited, DOX-induced cellular senescence. B7-H3 knockdown dramatically enhanced the growth arrest of CRC cells after low-dose DOX treatment, but B7-H3 overexpression had the opposite effect. By RNA-seq analysis and western blot, we showed that B7-H3 prevented cellular senescence and growth arrest through the AKT/TM4SF1/SIRT1 pathway. Blocking the AKT/TM4SF1/SIRT1 pathway dramatically reversed B7-H3-induced resistance to cellular senescence. More importantly, B7-H3 inhibited DOX-induced cellular senescence of CRC cells in vivo. Therefore, targeting B7-H3 or the B7-H3/AKT/TM4SF1/SIRT1 pathway might be a new strategy for promoting cellular senescence-like growth arrest during drug treatment in CRC. Nature Publishing Group UK 2021-05-06 /pmc/articles/PMC8102521/ /pubmed/33958586 http://dx.doi.org/10.1038/s41419-021-03736-2 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Wang, Ruoqin
Sun, Linqing
Xia, Suhua
Wu, Hongya
Ma, Yanchao
Zhan, Shenghua
Zhang, Guangbo
Zhang, Xueguang
Shi, Tongguo
Chen, Weichang
B7-H3 suppresses doxorubicin-induced senescence-like growth arrest in colorectal cancer through the AKT/TM4SF1/SIRT1 pathway
title B7-H3 suppresses doxorubicin-induced senescence-like growth arrest in colorectal cancer through the AKT/TM4SF1/SIRT1 pathway
title_full B7-H3 suppresses doxorubicin-induced senescence-like growth arrest in colorectal cancer through the AKT/TM4SF1/SIRT1 pathway
title_fullStr B7-H3 suppresses doxorubicin-induced senescence-like growth arrest in colorectal cancer through the AKT/TM4SF1/SIRT1 pathway
title_full_unstemmed B7-H3 suppresses doxorubicin-induced senescence-like growth arrest in colorectal cancer through the AKT/TM4SF1/SIRT1 pathway
title_short B7-H3 suppresses doxorubicin-induced senescence-like growth arrest in colorectal cancer through the AKT/TM4SF1/SIRT1 pathway
title_sort b7-h3 suppresses doxorubicin-induced senescence-like growth arrest in colorectal cancer through the akt/tm4sf1/sirt1 pathway
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8102521/
https://www.ncbi.nlm.nih.gov/pubmed/33958586
http://dx.doi.org/10.1038/s41419-021-03736-2
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