Evidence map›Paper›PMID 41844609›Full record

ArticleNature communications2026

Inhibition of the cancer stem cell immune checkpoint SOAT1 suppresses regulatory T cell functions through a trans-cellular 20(S)-Hydroxycholesterol-GPR132 pathway in mice.

Yahui Ding, Wanqi Fang, Ruiqing Xiang, Haitao Liu, Menglin Huang, Yingran Shen, Ying Chen, Guohao Wang, Zhaocai Zhou, Yun Ling and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Review
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

13 authors.

Yahui Ding *Department of Cell and Developmental Biology, School of Life Sciences and Zhongshan Hospital, Fudan University, Shanghai, 200438, China.
Wanqi Fang *Department of Cell and Developmental Biology, School of Life Sciences and Zhongshan Hospital, Fudan University, Shanghai, 200438, China.
Ruiqing Xiang *Department of Chemistry, Fudan University, Shanghai, 200438, China.
Haitao Liu *Department of Cell and Developmental Biology, School of Life Sciences and Zhongshan Hospital, Fudan University, Shanghai, 200438, China.
Menglin HuangDepartment of Cell and Developmental Biology, School of Life Sciences and Zhongshan Hospital, Fudan University, Shanghai, 200438, China.ORCID http://orcid.org/0009-0009-0245-4296
Yingran ShenShanghai Pulmonary Hospital Affiliated to Tongji University, Shanghai, 200433, China.
Ying ChenDepartment of Cell and Developmental Biology, School of Life Sciences and Zhongshan Hospital, Fudan University, Shanghai, 200438, China.
Guohao WangKey Laboratory of Genetic Evolution & Animal Models, and Key Laboratory of Animal Models & Human Disease Mechanisms of Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, 650201, Yunnan, China.
Zhaocai ZhouDepartment of Cell and Developmental Biology, School of Life Sciences and Zhongshan Hospital, Fudan University, Shanghai, 200438, China.ORCID http://orcid.org/0000-0002-5441-3922
Yun LingDepartment of Chemistry, Fudan University, Shanghai, 200438, China. yunling@fudan.edu.cn.
Ling V SunDepartment of Cell and Developmental Biology, School of Life Sciences and Zhongshan Hospital, Fudan University, Shanghai, 200438, China. lingsun@fudan.edu.cn.ORCID http://orcid.org/0000-0003-2410-793X
Yuetong WangDepartment of Cell and Developmental Biology, School of Life Sciences and Zhongshan Hospital, Fudan University, Shanghai, 200438, China. wangyt@fudan.edu.cn.ORCID http://orcid.org/0000-0003-3970-581X
Steven X HouDepartment of Cell and Developmental Biology, School of Life Sciences and Zhongshan Hospital, Fudan University, Shanghai, 200438, China. stevenhou@fudan.edu.cn.ORCID http://orcid.org/0000-0001-7583-2504

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although cancer immunotherapy has recently revolutionized treatment, the low response rate to existing immune checkpoint blockade (ICB) underscores the need for new druggable targets. Here, we find that SOAT1 is selectively expressed in cancer stem cell (CSC) and pharmacological inhibition with STK results in robust anti-tumor effects across various preclinical mouse models, including colon, liver, lung, breast, and melanoma cancer, with low toxicity. Mechanistically, treatment with STK (or gene knockdown of Soat1) induces the release of 20(S)-Hydroxycholesterol (20SOHC) from the tumor cells, and downstream activation of the trans-cellular 20SOHC (tumor)- GPR132 pathway in regulatory T cell (Treg), ultimately resulting in the suppression of Treg functions and enhanced dendritic cells and cytotoxic CD8

Indexed as

HydroxycholesterolsNeoplastic Stem CellsReceptors, G-Protein-CoupledT-Lymphocytes, RegulatoryAMP-Activated Protein KinasesAnimalsCell Line, TumorFemaleHumansImmune Checkpoint InhibitorsMiceMice, Inbred C57BLProtein Serine-Threonine KinasesSignal TransductionAMP-Activated Protein KinasesHydroxycholesterolsImmune Checkpoint InhibitorsProtein Serine-Threonine KinasesReceptors, G-Protein-CoupledStk11 protein, mouse

Identifiers

PMID41844609
PMCPMC13144448

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.