Evidence map›Paper›PMID 28481367›Full record

ArticleOncogenesis2017

Inhibition of malic enzyme 1 disrupts cellular metabolism and leads to vulnerability in cancer cells in glucose-restricted conditions.

S Murai, A Ando, S Ebara, M Hirayama, Y Satomi, T Hara

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
2.9field-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

50 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
  2. Malic enzyme 1 senses L-lactate to determine tumor heterogeneity.Signal transduction and targeted therapy · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Significance of Malic Enzyme 1 in Cancer: A Review.Current issues in molecular biology · 2025
    Review
  12. NADPCurrent medicinal chemistry · 2025
    Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

S MuraiOncology Drug Discovery Unit, Pharmaceutical Research Division, Takeda Pharmaceutical Company, Kanagawa, Japan.
A AndoIntegrated Technology Research Laboratories, Pharmaceutical Research Division, Takeda Pharmaceutical Company, Kanagawa, Japan.
S EbaraOncology Drug Discovery Unit, Pharmaceutical Research Division, Takeda Pharmaceutical Company, Kanagawa, Japan.
M HirayamaIntegrated Technology Research Laboratories, Pharmaceutical Research Division, Takeda Pharmaceutical Company, Kanagawa, Japan.
Y SatomiIntegrated Technology Research Laboratories, Pharmaceutical Research Division, Takeda Pharmaceutical Company, Kanagawa, Japan.
T HaraOncology Drug Discovery Unit, Pharmaceutical Research Division, Takeda Pharmaceutical Company, Kanagawa, Japan.
Takeda (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malic enzyme 1 (ME1) regulates one of the main pathways that provide nicotinamide adenine dinucleotide phosphate (NADPH), which is essential for cancer cell growth through maintenance of redox balance and biosynthesis processes in the cytoplasm. In this study, we found that ME1 inhibition disrupted metabolism in cancer cells and inhibited cancer cell growth by inducing senescence or apoptosis. In glucose-restricted culture conditions, cancer cells increased ME1 expression, and tracer experiments with labelled glutamine revealed that the flux of ME1-derived pyruvate to citrate was enhanced. In addition, cancer cells showed higher sensitivity to ME1 depletion in glucose-restricted conditions compared to normal culture conditions. These results suggest that in a low-glucose environment, where glycolysis and the pentose phosphate pathway (PPP) is attenuated, cancer cells become dependent on ME1 for the supply of NADPH and pyruvate. Our data demonstrate that ME1 is a promising target for cancer treatment, and a strategy using ME1 inhibitors combined with inhibition of glycolysis, PPP or redox balance regulators may provide an effective therapeutic option.

Identifiers

PMID28481367
PMCPMC5523067
OpenAlexW2611980624

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.