Evidence map›Paper›PMID 41521893›Full record

ArticleeLife2026

Chemotherapy resistance due to epithelial-to-mesenchymal transition is caused by abnormal lipid metabolic balance.

Atsushi Matsumoto, Akihito Inoko, Takuya Tanaka, Gen-Ichi Konishi, Waki Hosoda, Takahiro Kojima, Koji Ohnishi, Junichi Ikenouchi

Abstract read
In one paragraph

Article in eLife, 2026. 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. Article
  2. Review
  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.

Atsushi Matsumoto *Department of Biochemistry, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan.ORCID https://orcid.org/0000-0002-3814-3299
Akihito Inoko *Department of Pathology, Aichi Medical University School of Medicine, Nagakute, Japan.ORCID https://orcid.org/0000-0002-6739-2948
Takuya TanakaDepartment of Chemical Science and Engineering, Institute of Science Tokyo, Meguro-ku, Tokyo, Japan.
Gen-Ichi KonishiDepartment of Chemical Science and Engineering, Institute of Science Tokyo, Meguro-ku, Tokyo, Japan.
Waki HosodaDepartment of Pathology and Molecular Diagnostics, Aichi Cancer Center Hospital, Nagoya, Japan.
Takahiro KojimaDepartment of Urology, Aichi Cancer Center Hospital, Nagoya, Japan.
Koji OhnishiDepartment of Pathology, Aichi Medical University School of Medicine, Nagakute, Japan.
Junichi IkenouchiDepartment of Biochemistry, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan.ORCID https://orcid.org/0000-0002-2936-3548

Funding

Japan Agency for Medical Research and Development 21444781Japan Science and Technology Agency 10.52926/JPMJFR204LJapan Society for the Promotion of Science JP22KJ2374Japan Society for the Promotion of Science JP25H00994Japan Society for the Promotion of Science JP25H01325Japan Society for the Promotion of Science JP25K18465Japan Society for the Promotion of Science JP25K22454
6 · The paper itself

Abstract

Invasive cancer is defined by the loss of epithelial cell traits resulting from the ectopic expression of epithelial-mesenchymal transition (EMT)-related transcription factors such as Snail. Although EMT is known to impart chemoresistance to cancer cells, the precise molecular mechanisms remain elusive. We found that Snail expression confers chemoresistance by upregulating the cholesterol efflux pump ABCA1 as a countermeasure to the excess of cytotoxic free cholesterol relative to its major interaction partner in cellular membranes, sphingomyelin. This imbalance is introduced by the transcriptional repression of enzymes involved in the biosynthesis of sphingomyelin by Snail. Inhibiting esterification of cholesterol, which renders it inert, selectively suppresses growth of a xenograft model of Snail-positive kidney cancer. Our findings offer a new perspective on lipid-targeting strategies for invasive cancer therapy.

Indexed as

Antineoplastic AgentsDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionLipid MetabolismAnimalsATP Binding Cassette Transporter 1Cell Line, TumorCholesterolHumansMiceSnail Family Transcription FactorsSphingomyelinsABCA1 protein, humanAntineoplastic AgentsATP Binding Cassette Transporter 1CholesterolSnail Family Transcription FactorsSphingomyelinscancercell biologychemotherapycholesterolepithelial–mesenchymal transitionhumanmouseSnailsphingomyelin

Identifiers

PMID41521893
PMCPMC12795503

What Socratic holds

Textmetadata
LicenceCC BY
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.