Evidence map›Paper›PMID 42397900›Full record

ArticleScience advances2026

A targetable FTO/SLC7A11/CBS/CTH axis controls cysteine metabolism, growth and survival in NSCLC.

Nishanth Kuganesan, Margaret Pan, Haowen Jiang, Stavros Melemenidis, Jiangbin Ye, Sara Richter, Maximillian Diehn, Kerriann M Casey, Edward E Graves, Quynh Thu Le and 1 more

Abstract read
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In one paragraph

Article in Science advances, 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

11 authors.

Nishanth KuganesanDepartment of Radiation Oncology, Stanford University, Stanford, CA 94305, USA.ORCID 0009-0001-0370-4068
Margaret PanDepartment of Radiation Oncology, Stanford University, Stanford, CA 94305, USA.
Haowen JiangDepartment of Radiation Oncology, Stanford University, Stanford, CA 94305, USA.ORCID 0000-0003-4021-3820
Stavros MelemenidisDepartment of Radiation Oncology, Stanford University, Stanford, CA 94305, USA.ORCID 0000-0002-3941-8784
Jiangbin YeDepartment of Radiation Oncology, Stanford University, Stanford, CA 94305, USA.ORCID 0000-0003-1117-4869
Sara RichterDepartment of Radiation Oncology, Stanford University, Stanford, CA 94305, USA.ORCID 0000-0003-1643-691X
Maximillian DiehnDepartment of Radiation Oncology, Stanford University, Stanford, CA 94305, USA.ORCID 0000-0003-2032-0581
Kerriann M CaseyDepartment of Comparative Medicine, Stanford University, Stanford, CA 94305, USA.ORCID 0000-0003-4228-928X
Edward E GravesDepartment of Radiation Oncology, Stanford University, Stanford, CA 94305, USA.ORCID 0000-0003-4265-9041
Quynh Thu LeDepartment of Radiation Oncology, Stanford University, Stanford, CA 94305, USA.ORCID 0000-0002-3682-1439
Erinn B RankinDepartment of Radiation Oncology, Stanford University, Stanford, CA 94305, USA.ORCID 0000-0002-2045-2296

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cysteine metabolism plays a crucial role in the growth and survival of non-small cell lung cancer (NSCLC), although the mechanisms governing its regulation are not fully understood. Here, we demonstrate that the RNA demethylase FTO is a therapeutic target that drives cysteine metabolism in NSCLC cells. Genetic or pharmacologic inhibition of FTO reduced cystine uptake and transsulfuration activity, leading to depleted intracellular glutathione, elevated reactive oxygen species (ROS), and ROS-mediated DNA damage and cell death. Mechanistically, FTO promotes the expression of the cystine uptake transporter SLC7A11 and the transsulfuration enzymes cystathionine β-synthase (CBS) and cystathionine γ-lyase (CTH) to promote NSCLC cystine uptake, transsulfuration activity, and survival. FTO inhibition increased lipid peroxidation, reduced tumor growth, and resulted in additive therapeutic benefit in combination with radiotherapy in multiple NSCLC xenograft models. Collectively, our study reveals a role for FTO in cysteine metabolism and highlights the therapeutic potential of targeting cancer epitranscriptomics and cysteine metabolism for NSCLC therapy.

Indexed as

Alpha-Ketoglutarate-Dependent Dioxygenase FTOAmino Acid Transport System y+Carcinoma, Non-Small-Cell LungCystathionine beta-SynthaseCystathionine gamma-LyaseCysteineLung NeoplasmsAnimalsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansMiceReactive Oxygen SpeciesXenograft Model Antitumor AssaysAlpha-Ketoglutarate-Dependent Dioxygenase FTOAmino Acid Transport System y+Cystathionine beta-SynthaseCystathionine gamma-LyaseCysteineFTO protein, humanReactive Oxygen SpeciesSLC7A11 protein, human

Identifiers

PMID42397900
PMCPMC13330832

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.