Evidence map›Paper›PMID 35883815›Full record

ReviewAntioxidants (Basel, Switzerland)2022

Metabolic Adaptation-Mediated Cancer Survival and Progression in Oxidative Stress.

Yongquan Tang, Zhe Zhang, Yan Chen, Siyuan Qin, Li Zhou, Wei Gao, Zhisen Shen

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 27 citations in OpenAlex.

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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 at 4 institutions in 1 country.

Yongquan TangDepartment of Pediatric Surgery, West China Hospital, Sichuan University, Chengdu 610041, China.
Zhe ZhangState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Collaborative Innovation Center for Biotherapy, Chengdu 610041, China.
Yan ChenState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Collaborative Innovation Center for Biotherapy, Chengdu 610041, China.
Siyuan QinState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Collaborative Innovation Center for Biotherapy, Chengdu 610041, China.
Li ZhouState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Collaborative Innovation Center for Biotherapy, Chengdu 610041, China.
Wei GaoClinical Medical College & Affiliated Hospital of Chengdu University, Chengdu University, Chengdu 610106, China.
Zhisen ShenDepartment of Otorhinolaryngology and Head and Neck Surgery, The Affiliated Lihuili Hospital, Ningbo University, Ningbo 315040, China.
Sichuan University · CNChengdu University · CNNingbo Medical Center Lihuili Hospital · CNState Key Laboratory of Biotherapy

Funding

Chengdu Science and Technology Program 2019-YF05-00715-SNChina Postdoctoral Science Foundation 220M673208National Natural Science Foundation of China 82003113, 82102738, 31971104Ningbo Medical and Health Brand Discipline PPXK2018-02Post-Doctor Research Project, West China Hospital, Sichuan University 2020HXBH039The Fundamental Research Funds for the Central Universities 2020SCU12025
6 · The paper itself

Abstract

Undue elevation of ROS levels commonly occurs during cancer evolution as a result of various antitumor therapeutics and/or endogenous immune response. Overwhelming ROS levels induced cancer cell death through the dysregulation of ROS-sensitive glycolytic enzymes, leading to the catastrophic depression of glycolysis and oxidative phosphorylation (OXPHOS), which are critical for cancer survival and progression. However, cancer cells also adapt to such catastrophic oxidative and metabolic stresses by metabolic reprograming, resulting in cancer residuality, progression, and relapse. This adaptation is highly dependent on NADPH and GSH syntheses for ROS scavenging and the upregulation of lipolysis and glutaminolysis, which fuel tricarboxylic acid cycle-coupled OXPHOS and biosynthesis. The underlying mechanism remains poorly understood, thus presenting a promising field with opportunities to manipulate metabolic adaptations for cancer prevention and therapy. In this review, we provide a summary of the mechanisms of metabolic regulation in the adaptation of cancer cells to oxidative stress and the current understanding of its regulatory role in cancer survival and progression.

Indexed as

cancer stemnessmetabolic adaptationmetabolic reprogrammingoxidative stresstumor metastasis

Identifiers

PMID35883815
PMCPMC9311581
OpenAlexW4284706722

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.