Evidence map›Paper›PMID 39996805›Full record

ReviewCurrent issues in molecular biology2025

Significance of Malic Enzyme 1 in Cancer: A Review.

Rina Fujiwara-Tani, Chie Nakashima, Hitoshi Ohmori, Kiyomu Fujii, Yi Luo, Takamitsu Sasaki, Ruiko Ogata, Hiroki Kuniyasu

Abstract readReview
In one paragraph

Review in Current issues in molecular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. A cryptic allosteric pocket shapes isoform-selective inhibition of human malic enzymes.Protein science : a publication of the Protein Society · 2026
    Article
  2. Article
  3. Article
  4. Article
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.

Rina Fujiwara-TaniDepartment of Molecular Pathology, Nara Medical University School of Medicine, 840 Shijo-cho, Kashihara 634-8521, Japan.
Chie NakashimaDepartment of Molecular Pathology, Nara Medical University School of Medicine, 840 Shijo-cho, Kashihara 634-8521, Japan.
Hitoshi OhmoriDepartment of Molecular Pathology, Nara Medical University School of Medicine, 840 Shijo-cho, Kashihara 634-8521, Japan.
Kiyomu FujiiDepartment of Molecular Pathology, Nara Medical University School of Medicine, 840 Shijo-cho, Kashihara 634-8521, Japan.
Yi LuoDepartment of Molecular Pathology, Nara Medical University School of Medicine, 840 Shijo-cho, Kashihara 634-8521, Japan.
Takamitsu SasakiDepartment of Molecular Pathology, Nara Medical University School of Medicine, 840 Shijo-cho, Kashihara 634-8521, Japan.
Ruiko OgataDepartment of Molecular Pathology, Nara Medical University School of Medicine, 840 Shijo-cho, Kashihara 634-8521, Japan.
Hiroki KuniyasuDepartment of Molecular Pathology, Nara Medical University School of Medicine, 840 Shijo-cho, Kashihara 634-8521, Japan.ORCID 0000-0003-2298-8825

Funding

Ministry of Education, Culture, Sports, Science and Technology 19K16564Ministry of Education, Culture, Sports, Science and Technology 19K19332Ministry of Education, Culture, Sports, Science and Technology 20K21659
6 · The paper itself

Abstract

Malic enzyme 1 (ME1) plays a key role in promoting malignant phenotypes in various types of cancer. ME1 promotes epithelial-mesenchymal transition (EMT) and enhances stemness via glutaminolysis, energy metabolism reprogramming from oxidative phosphorylation to glycolysis. As a result, ME1 promotes the malignant phenotypes of cancer cells and poor patient prognosis. In particular, ME1 expression is promoted in hypoxic environments associated with hypoxia-inducible factor (HIF1) α. ME1 is overexpressed in budding cells at the cancer invasive front, promoting cancer invasion and metastasis. ME1 also generates nicotinamide adenine dinucleotide (NADPH), which, together with glucose-6-phosphate dehydrogenase (G6PD) and isocitrate dehydrogenase (IDH1), expands the NADPH pool, maintaining the redox balance in cancer cells, suppressing cell death by neutralizing mitochondrial reactive oxygen species (ROS), and promoting stemness. This review summarizes the latest research insights into the mechanisms by which ME1 contributes to cancer progression. Because ME1 is involved in various aspects of cancer and promotes many of its malignant phenotypes, it is expected that ME1 will become a novel drug target in the near future.

Indexed as

cancer stem cellsenergy metabolismepithelial–mesenchymal transitionhypoxiamalic enzyme 1

Identifiers

PMID39996805
PMCPMC11854147

What OpenQuestion holds

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Registered trials

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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.