Evidence map›Paper›PMID 36154922›Full record

ReviewJournal of biomedical science2022

Mitochondrial oxidative stress in the tumor microenvironment and cancer immunoescape: foe or friend?

Cheng-Liang Kuo, Ananth Ponneri Babuharisankar, Ying-Chen Lin, Hui-Wen Lien, Yu Kang Lo, Han-Yu Chou, Vidhya Tangeda, Li-Chun Cheng, An Ning Cheng, Alan Yueh-Luen Lee

Open access · diamondAbstract readReview
In one paragraph

Review in Journal of biomedical science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 216 papers.

0numbers the graph read from it
0cells of the map it votes in
216citing papers in PubMed
30.3field-weighted citation impact, top 1% 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

216 citing papers in PubMed, 330 citations in OpenAlex.

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156 more citing papers are in PubMed but not listed here.

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

10 authors at 4 institutions in 1 country.

Cheng-Liang Kuo *National Institute of Cancer Research, National Health Research Institutes, 35 Keyan Road, Zhunan, Miaoli, 35053, Taiwan.
Ananth Ponneri Babuharisankar *National Institute of Cancer Research, National Health Research Institutes, 35 Keyan Road, Zhunan, Miaoli, 35053, Taiwan.
Ying-Chen LinNational Institute of Cancer Research, National Health Research Institutes, 35 Keyan Road, Zhunan, Miaoli, 35053, Taiwan.
Hui-Wen LienNational Institute of Cancer Research, National Health Research Institutes, 35 Keyan Road, Zhunan, Miaoli, 35053, Taiwan.
Yu Kang LoNational Institute of Cancer Research, National Health Research Institutes, 35 Keyan Road, Zhunan, Miaoli, 35053, Taiwan.
Han-Yu ChouNational Institute of Cancer Research, National Health Research Institutes, 35 Keyan Road, Zhunan, Miaoli, 35053, Taiwan.
Vidhya TangedaNational Institute of Cancer Research, National Health Research Institutes, 35 Keyan Road, Zhunan, Miaoli, 35053, Taiwan.
Li-Chun ChengLiver Research Center, Linkou Chang Gung Memorial Hospital, Taoyuan, 333, Taiwan.
An Ning ChengGenomics Research Center, Academia Sinica, Taipei, 115, Taiwan.
Alan Yueh-Luen LeeNational Institute of Cancer Research, National Health Research Institutes, 35 Keyan Road, Zhunan, Miaoli, 35053, Taiwan. alanylee@nhri.edu.tw.ORCID http://orcid.org/0000-0003-0252-0571
National Health Research Institutes · TWGenomics Research Center, Academia Sinica · TWKaohsiung Medical University · TWLinkou Chang Gung Memorial Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The major concept of "oxidative stress" is an excess elevated level of reactive oxygen species (ROS) which are generated from vigorous metabolism and consumption of oxygen. The precise harmonization of oxidative stresses between mitochondria and other organelles in the cell is absolutely vital to cell survival. Under oxidative stress, ROS produced from mitochondria and are the major mediator for tumorigenesis in different aspects, such as proliferation, migration/invasion, angiogenesis, inflammation, and immunoescape to allow cancer cells to adapt to the rigorous environment. Accordingly, the dynamic balance of oxidative stresses not only orchestrate complex cell signaling events in cancer cells but also affect other components in the tumor microenvironment (TME). Immune cells, such as M2 macrophages, dendritic cells, and T cells are the major components of the immunosuppressive TME from the ROS-induced inflammation. Based on this notion, numerous strategies to mitigate oxidative stresses in tumors have been tested for cancer prevention or therapies; however, these manipulations are devised from different sources and mechanisms without established effectiveness. Herein, we integrate current progress regarding the impact of mitochondrial ROS in the TME, not only in cancer cells but also in immune cells, and discuss the combination of emerging ROS-modulating strategies with immunotherapies to achieve antitumor effects.

Indexed as

NeoplasmsTumor MicroenvironmentHumansInflammationOxidative StressOxygenReactive Oxygen SpeciesOxygenReactive Oxygen SpeciesCisplatin resistanceCombination cancer immunotherapyHypoxiaImmunoescapeInflammationLon protease (LonP1)Mitochondrial chaperoneMitochondrial reactive oxygen species (mtROS)Tumor microenvironment

Identifiers

PMID36154922
PMCPMC9511749
OpenAlexW4297198373

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.