Evidence mapPaperPMID 37792154Full record

ReviewCellular oncology (Dordrecht, Netherlands)2024

Redox signaling-mediated tumor extracellular matrix remodeling: pleiotropic regulatory mechanisms.

Guowen Liu, Bowen Li, Siyuan Qin, Edouard C Nice, Jinlin Yang, Li Yang, Canhua Huang

Abstract readReview
In one paragraph

Review in Cellular oncology (Dordrecht, Netherlands), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

6 citing papers in PubMed, 13 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 2 countries.

Guowen Liu *State Key Laboratory of Biotherapy and Cancer Center, Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, and , Chengdu, 610041, China.
Bowen Li *State Key Laboratory of Biotherapy and Cancer Center, Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, and , Chengdu, 610041, China.
Siyuan Qin *State Key Laboratory of Biotherapy and Cancer Center, Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, and , Chengdu, 610041, China.
Edouard C NiceDepartment of Biochemistry and Molecular Biology, Monash University, Clayton, VIC, 3800, Australia.
Jinlin YangDepartment of Gastroenterology & Hepatology, West China Hospital of Sichuan University, Sichuan Province, No.37 Guoxue Alley, Chengdu, 610041, China. mouse-577@163.com.
Li YangDepartment of Gastroenterology & Hepatology, West China Hospital of Sichuan University, Sichuan Province, No.37 Guoxue Alley, Chengdu, 610041, China. yangli_hx@scu.edu.cn.
Canhua HuangState Key Laboratory of Biotherapy and Cancer Center, Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, and , Chengdu, 610041, China. hcanhua@scu.edu.cn.
State Key Laboratory of BiotherapySichuan University · CNMonash University · AUWest China Hospital of Sichuan University · CN

Funding

1·3·5 project for disciplines of excellence, West China Hospital, Sichuan University ZYGD22007
6 · The paper itself

Abstract

backgroundThe extracellular matrix (ECM), a fundamental constituent of all tissues and organs, is crucial for shaping the tumor microenvironment. Dysregulation of ECM remodeling has been closely linked to tumor initiation and progression, where specific signaling pathways, including redox signaling, play essential roles. Reactive oxygen species (ROS) are risk factors for carcinogenesis whose excess can facilitate the oxidative damage of biomacromolecules, such as DNA and proteins. Emerging evidence suggests that redox effects can aid the modification, stimulation, and degradation of ECM, thus affecting ECM remodeling. These alterations in both the density and components of the ECM subsequently act as critical drivers for tumorigenesis. In this review, we provide an overview of the functions and primary traits of the ECM, and it delves into our current understanding of how redox reactions participate in ECM remodeling during cancer progression. We also discuss the opportunities and challenges presented by clinical strategies targeting redox-controlled ECM remodeling to overcome cancer.

conclusionsThe redox-mediated ECM remodeling contributes importantly to tumor survival, progression, metastasis, and poor prognosis. A comprehensive investigation of the concrete mechanism of redox-mediated tumor ECM remodeling and the combination usage of redox-targeted drugs with existing treatment means may reveal new therapeutic strategy for future antitumor therapies.

Indexed as

Extracellular MatrixNeoplasmsOxidation-ReductionSignal TransductionAnimalsHumansReactive Oxygen SpeciesTumor MicroenvironmentReactive Oxygen SpeciesAntioxidantsCancer therapyECM remodelingOxidative stressReactive oxygen species

Identifiers

PMID37792154
PMCPMC12974085
OpenAlexW4387327194

What Socratic holds

Textmetadata
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 Socratic graph.