Evidence map›Paper›PMID 42174510›Full record

ArticleBMC cancer2026

Role of glutathione disulfide reductase in colorectal cancer: a tumor suppressor.

Lilin Lin, Zexiu Chen, Cong-Yu Zhang, Jingnian Fang

Abstract read
In one paragraph

Article in BMC cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

4 authors.

Lilin Lin *Department of Neurology, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong Province, 515041, China.
Zexiu Chen *Department of Medical Ultrasound, The First Affiliated Hospital of Shantou University Medical College, Shantou, 515041, China.
Cong-Yu ZhangCancer Center, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning Province, 121001, China.
Jingnian FangDepartment of Neurology, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong Province, 515041, China. 447437164_2006@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGlutathione-disulfide reductase (GSR) was responsible for maintaining the supply of reduced glutathione, and was found to be abnormally expressed in a variety of cancers. There was an incomplete understanding regarding the roles of GSR in colorectal cancer (CRC) today.

methodsWe used colorectal cancer tissues and cell lines to detect the function of GSR in CRC. We also used bioinformatics to analyze the related pathways of GSR in colorectal cancer.

resultsGSR mRNA was down-regulated in CRC (p < 0.05). The expression of GSR mRNA with T3 and T4 patients was lower than that with T1 and T2 patients, with M1 patients was lower than that with M0 patients, with N1 and N2 patients was lower than that with N0 stage patients, with stage 3 and stage 4 patients was lower than that with stage1 and stage 2 patients (p < 0.05). Overall survival (OS), disease-specific survival (DSS), progression survival (PFS), post-progression survival (PPS) and recurrence-free survival (RFS) time for patients with high expression of GSR was higher than that for patients with low GSR expression (p < 0.05). The expression of p-p38 MAPK and p-ERK increased in GSR knockdown cells, while the expression of p-Nrf2, KEAP1, p-PI3K and p-Akt decreased. Consistent with alterations in the MAPK/ERK signaling pathway, cells with GSR knockdown exhibited significantly enhanced proliferative, migratory, and invasive capabilities, along with increased ROS production (all p < 0.001), while showing a reduced apoptosis rate (p < 0.001). Furthermore, both re-expression of GSR and treatment with an ERK inhibitor effectively reversed the phenotypic and molecular changes induced by GSR knockdown.

conclusionThe expression of GSR was closely related to the development of colorectal cancer. GSR was low expressed and played a tumor-suppressive role through inhibiting the production of ROS, and the activation of p38 MAPK/ERK pathways in CRC. GSR has the potential to become a potential biomarker for the diagnosis and treatment of colorectal cancer.

Indexed as

Colorectal NeoplasmsGlutathione ReductaseAgedApoptosisCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHumansMaleMiddle AgedSignal TransductionGlutathione ReductaseBioinformatics analysisColorectal cancerGSRTumor suppressor gene

Identifiers

PMID42174510
PMCPMC13371517

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.