Evidence map›Paper›PMID 26956544›Full record

ArticleScientific reports2016

Redox homeostasis protects mitochondria through accelerating ROS conversion to enhance hypoxia resistance in cancer cells.

Pengying Li, Dongyang Zhang, Lingxiao Shen, Kelei Dong, Meiling Wu, Zhouluo Ou, Dongyun Shi

Abstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
–field-weighted citation impact
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

43 citing papers in PubMed.

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  9. Expression Changes of SIRT1 and FOXO3a Significantly Correlate with Oxidative Stress Resistance Genes in AML Patients.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2023
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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

7 authors.

Pengying LiDepartment of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Shanghai 200032, People's Republic of China.
Dongyang ZhangDepartment of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Shanghai 200032, People's Republic of China.
Lingxiao ShenDepartment of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Shanghai 200032, People's Republic of China.
Kelei DongDepartment of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Shanghai 200032, People's Republic of China.
Meiling WuDepartment of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Shanghai 200032, People's Republic of China.
Zhouluo OuCancer Research Institute of Fudan University Shanghai Cancer Center, Shanghai 200032, People's Republic of China.
Dongyun ShiDepartment of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Shanghai 200032, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are the powerhouses of eukaryotic cells and the main source of reactive oxygen species (ROS) in hypoxic cells, participating in regulating redox homeostasis. The mechanism of tumor hypoxia tolerance, especially the role of mitochondria in tumor hypoxia resistance remains largely unknown. This study aimed to explore the role of mitochondria in tumor hypoxia resistance. We observed that glycolysis in hypoxic cancer cells was up-regulated more rapidly, with far lesser attenuation in aerobic oxidation, thus contributing to a more stable ATP/ADP ratio. In hypoxia, cancer cells rapidly convert hypoxia-induced O(2˙)(-) into H2O2. H2O2 is further decomposed by a relatively stronger antioxidant system, causing ROS levels to increase lesser compared to normal cells. The moderate ROS leads to an appropriate degree of autophagy, eliminating the damaged mitochondria and offering nutrients to promote mitochondria fusion, thus protects mitochondria and improves hypoxia tolerance in cancer. The functional mitochondria could enable tumor cells to flexibly switch between glycolysis and oxidative phosphorylation to meet the different physiological requirements during the hypoxia/re-oxygenation cycling of tumor growth.

Indexed as

HomeostasisTumor HypoxiaAerobiosisCell Line, TumorGlycolysisHumansMitochondriaOxidation-ReductionOxidative PhosphorylationReactive Oxygen SpeciesReactive Oxygen Species

Identifiers

PMID26956544
PMCPMC4783784

What OpenQuestion holds

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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.