Hyperbaric oxygen suppressed tumor progression through the improvement of tumor hypoxia and induction of tumor apoptosis in A549-cell-transferred lung cancer

Abstract Tumor cells have long been recognized as a relative contraindication to hyperbaric oxygen treatment (HBOT) since HBOT might enhance progressive cancer growth. However, in an oxygen deficit condition, tumor cells are more progressive and can be metastatic. HBOT increasing in oxygen partial p...

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Autores principales: Shao-Yuan Chen, Koichi Tsuneyama, Mao-Hsiung Yen, Jiunn-Tay Lee, Jiun-Liang Chen, Shih-Ming Huang
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Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/f26e2770b09044729fa799a8bfd30b08
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spelling oai:doaj.org-article:f26e2770b09044729fa799a8bfd30b082021-12-02T15:03:07ZHyperbaric oxygen suppressed tumor progression through the improvement of tumor hypoxia and induction of tumor apoptosis in A549-cell-transferred lung cancer10.1038/s41598-021-91454-22045-2322https://doaj.org/article/f26e2770b09044729fa799a8bfd30b082021-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-91454-2https://doaj.org/toc/2045-2322Abstract Tumor cells have long been recognized as a relative contraindication to hyperbaric oxygen treatment (HBOT) since HBOT might enhance progressive cancer growth. However, in an oxygen deficit condition, tumor cells are more progressive and can be metastatic. HBOT increasing in oxygen partial pressure may benefit tumor suppression. In this study, we investigated the effects of HBOT on solid tumors, such as lung cancer. Non-small cell human lung carcinoma A549-cell-transferred severe combined immunodeficiency mice (SCID) mice were selected as an in vivo model to detect the potential mechanism of HBOT in lung tumors. HBOT not only improved tumor hypoxia but also suppressed tumor growth in murine xenograft tumor models. Platelet endothelial cell adhesion molecule (PECAM-1/CD31) was significantly increased after HBOT. Immunostaining of cleaved caspase-3 was demonstrated and apoptotic tumor cells with nuclear debris were aggregated starting on the 14th-day after HBOT. In vitro, HBOT suppressed the growth of A549 cells in a time-dependent manner and immediately downregulated the expression of p53 protein after HBOT in A549 cells. Furthermore, HBOT-reduced p53 protein could be rescued by a proteasome degradation inhibitor, but not an autophagy inhibitor in A549 cells. Our results demonstrated that HBOT improved tissue angiogenesis, tumor hypoxia and increased tumor apoptosis to lung cancer cells in murine xenograft tumor models, through modifying the tumor hypoxic microenvironment. HBOT will merit further cancer therapy as an adjuvant treatment for solid tumors, such as lung cancer.Shao-Yuan ChenKoichi TsuneyamaMao-Hsiung YenJiunn-Tay LeeJiun-Liang ChenShih-Ming HuangNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-15 (2021)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Shao-Yuan Chen
Koichi Tsuneyama
Mao-Hsiung Yen
Jiunn-Tay Lee
Jiun-Liang Chen
Shih-Ming Huang
Hyperbaric oxygen suppressed tumor progression through the improvement of tumor hypoxia and induction of tumor apoptosis in A549-cell-transferred lung cancer
description Abstract Tumor cells have long been recognized as a relative contraindication to hyperbaric oxygen treatment (HBOT) since HBOT might enhance progressive cancer growth. However, in an oxygen deficit condition, tumor cells are more progressive and can be metastatic. HBOT increasing in oxygen partial pressure may benefit tumor suppression. In this study, we investigated the effects of HBOT on solid tumors, such as lung cancer. Non-small cell human lung carcinoma A549-cell-transferred severe combined immunodeficiency mice (SCID) mice were selected as an in vivo model to detect the potential mechanism of HBOT in lung tumors. HBOT not only improved tumor hypoxia but also suppressed tumor growth in murine xenograft tumor models. Platelet endothelial cell adhesion molecule (PECAM-1/CD31) was significantly increased after HBOT. Immunostaining of cleaved caspase-3 was demonstrated and apoptotic tumor cells with nuclear debris were aggregated starting on the 14th-day after HBOT. In vitro, HBOT suppressed the growth of A549 cells in a time-dependent manner and immediately downregulated the expression of p53 protein after HBOT in A549 cells. Furthermore, HBOT-reduced p53 protein could be rescued by a proteasome degradation inhibitor, but not an autophagy inhibitor in A549 cells. Our results demonstrated that HBOT improved tissue angiogenesis, tumor hypoxia and increased tumor apoptosis to lung cancer cells in murine xenograft tumor models, through modifying the tumor hypoxic microenvironment. HBOT will merit further cancer therapy as an adjuvant treatment for solid tumors, such as lung cancer.
format article
author Shao-Yuan Chen
Koichi Tsuneyama
Mao-Hsiung Yen
Jiunn-Tay Lee
Jiun-Liang Chen
Shih-Ming Huang
author_facet Shao-Yuan Chen
Koichi Tsuneyama
Mao-Hsiung Yen
Jiunn-Tay Lee
Jiun-Liang Chen
Shih-Ming Huang
author_sort Shao-Yuan Chen
title Hyperbaric oxygen suppressed tumor progression through the improvement of tumor hypoxia and induction of tumor apoptosis in A549-cell-transferred lung cancer
title_short Hyperbaric oxygen suppressed tumor progression through the improvement of tumor hypoxia and induction of tumor apoptosis in A549-cell-transferred lung cancer
title_full Hyperbaric oxygen suppressed tumor progression through the improvement of tumor hypoxia and induction of tumor apoptosis in A549-cell-transferred lung cancer
title_fullStr Hyperbaric oxygen suppressed tumor progression through the improvement of tumor hypoxia and induction of tumor apoptosis in A549-cell-transferred lung cancer
title_full_unstemmed Hyperbaric oxygen suppressed tumor progression through the improvement of tumor hypoxia and induction of tumor apoptosis in A549-cell-transferred lung cancer
title_sort hyperbaric oxygen suppressed tumor progression through the improvement of tumor hypoxia and induction of tumor apoptosis in a549-cell-transferred lung cancer
publisher Nature Portfolio
publishDate 2021
url https://doaj.org/article/f26e2770b09044729fa799a8bfd30b08
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AT maohsiungyen hyperbaricoxygensuppressedtumorprogressionthroughtheimprovementoftumorhypoxiaandinductionoftumorapoptosisina549celltransferredlungcancer
AT jiunntaylee hyperbaricoxygensuppressedtumorprogressionthroughtheimprovementoftumorhypoxiaandinductionoftumorapoptosisina549celltransferredlungcancer
AT jiunliangchen hyperbaricoxygensuppressedtumorprogressionthroughtheimprovementoftumorhypoxiaandinductionoftumorapoptosisina549celltransferredlungcancer
AT shihminghuang hyperbaricoxygensuppressedtumorprogressionthroughtheimprovementoftumorhypoxiaandinductionoftumorapoptosisina549celltransferredlungcancer
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