Evidence map›Paper›PMID 34103583›Full record

ArticleScientific reports2021

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

Shao-Yuan Chen, Koichi Tsuneyama, Mao-Hsiung Yen, Jiunn-Tay Lee, Jiun-Liang Chen, Shih-Ming Huang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.5field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 38 citations in OpenAlex.

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  13. Effects of hypoxia on the growth of gastric cancer and the chemotherapeutic efficacy of 5-fluorouracil.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 2 countries.

Shao-Yuan ChenDepartment of Hyperbaric Medicine and Neurology, Cardinal Tien Hospital, New Taipei City, Taiwan, ROC. 1sychen@yahoo.com.tw.
Koichi TsuneyamaDepartment of Molecular and Environmental Pathology, The University of Tokushima, Tokushima, Japan.
Mao-Hsiung YenDepartment of Pharmacology, National Defense Medical Center, Taipei, Taiwan, ROC.
Jiunn-Tay LeeDepartment of Neurology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, ROC.
Jiun-Liang ChenDepartment of Traditional Chinese Medicine, Chang Gung University, Taoyuan City, Taiwan, ROC.
Shih-Ming HuangDepartment of Biochemistry, National Defense Medical Center, Taipei, Taiwan, ROC.
National Defense Medical Center · TWCardinal Tien Hospital · TWChang Gung University · TWTokushima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

ApoptosisTumor HypoxiaA549 CellsAnimalsCarcinoma, Non-Small-Cell LungCaspase 3Cell Line, TumorDisease ProgressionFemaleHumansHyperbaric OxygenationHypoxiaImmunohistochemistryLung NeoplasmsMiceMice, SCIDCaspase 3PECAM1 protein, humanPlatelet Endothelial Cell Adhesion Molecule-1Proteasome Endopeptidase Complex

Identifiers

PMID34103583
PMCPMC8187442
OpenAlexW3171867299

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.