Evidence map›Paper›PMID 38723197›Full record

ArticleRedox report : communications in free radical research2024

MTHFD2-mediated redox homeostasis promotes gastric cancer progression under hypoxic conditions.

Hai-Yu Mo, Ruo-Bing Wang, Meng-Yao Ma, Yi Zhang, Xin-Yu Li, Wang-Rong Wen, Yi Han, Tian Tian

Abstract read
In one paragraph

Article in Redox report : communications in free radical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. MTHFD2: a promising metabolic checkpoint for diseases.Journal of translational medicine · 2026
    Review
  5. Article
  6. Mitochondrial Stress inAntioxidants (Basel, Switzerland) · 2026
    Review
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  8. Article
  9. Article
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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

8 authors.

Hai-Yu MoDepartment of Medical Biochemistry and Molecular Biology, School of Medicine, Jinan University, Guangzhou, People's Republic of China.
Ruo-Bing WangDepartment of Medical Biochemistry and Molecular Biology, School of Medicine, Jinan University, Guangzhou, People's Republic of China.
Meng-Yao MaDepartment of Medical Biochemistry and Molecular Biology, School of Medicine, Jinan University, Guangzhou, People's Republic of China.
Yi ZhangState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University, Guangzhou, People's Republic of China.
Xin-Yu LiDepartment of Medical Biochemistry and Molecular Biology, School of Medicine, Jinan University, Guangzhou, People's Republic of China.
Wang-Rong WenClinical Laboratory, The Affiliated Shunde Hospital of Jinan University, Foshan, People's Republic of China.
Yi HanState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University, Guangzhou, People's Republic of China.
Tian TianDepartment of Medical Biochemistry and Molecular Biology, School of Medicine, Jinan University, Guangzhou, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesCancer cells undergo metabolic reprogramming to adapt to high oxidative stress, but little is known about how metabolic remodeling enables gastric cancer cells to survive stress associated with aberrant reactive oxygen species (ROS) production. Here, we aimed to identify the key metabolic enzymes that protect gastric cancer (GC) cells from oxidative stress.

methodsROS level was detected by DCFH-DA probes. Multiple cell biological studies were performed to identify the underlying mechanisms. Furthermore, cell-based xenograft and patient-derived xenograft (PDX) model were performed to evaluate the role of MTHFD2 in vivo.

resultsWe found that overexpression of MTHFD2, but not MTHFD1, is associated with reduced overall and disease-free survival in gastric cancer. In addition, MTHFD2 knockdown reduces the cellular NADPH/NADP+ ratio, colony formation and mitochondrial function, increases cellular ROS and cleaved PARP levels and induces in cell death under hypoxia, a hallmark of solid cancers and a common inducer of oxidative stress. Moreover, genetic or pharmacological inhibition of MTHFD2 reduces tumor burden in both tumor cell lines and patient-derived xenograft-based models. DISCUSSION: our study highlights the crucial role of MTHFD2 in redox regulation and tumor progression, demonstrating the therapeutic potential of targeting MTHFD2.

Indexed as

Disease ProgressionHomeostasisMethylenetetrahydrofolate Dehydrogenase (NADP)Oxidative StressStomach NeoplasmsAminohydrolasesAnimalsCell Line, TumorHumansMiceMultifunctional EnzymesOxidation-ReductionReactive Oxygen SpeciesXenograft Model Antitumor AssaysAminohydrolasesMethylenetetrahydrofolate Dehydrogenase (NADP)MTHFD2 protein, humanMultifunctional EnzymesReactive Oxygen SpeciesGastric cancermethylene tetrahydrofolate dehydrogenase 2 (MTHFD2)NADPHreactive oxygen species (ROS)redox metabolism

Identifiers

PMID38723197
PMCPMC11086033

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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.