Evidence map›Paper›PMID 40307212›Full record

ArticleNature communications2025

Inhibition of MBTPS1 enhances antitumor immunity and potentiates anti-PD-1 immunotherapy.

Yi-Yu Wang, Jin-Fei Lin, Wen-Wei Wu, Zhe Fu, Fen Cao, Yan-Xing Chen, Hai-Yu Mo, Hui Sheng, Ze-Xian Liu, Zhao-Lei Zeng and 4 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. 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

14 authors.

Yi-Yu Wang *Department of Medical Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University, Guangzhou, 510060, P. R. China.
Jin-Fei Lin *Department of Medical Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University, Guangzhou, 510060, P. R. China.
Wen-Wei Wu *Department of Medical Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University, Guangzhou, 510060, P. R. China.
Zhe Fu *Department of Medical Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University, Guangzhou, 510060, P. R. China.
Fen CaoDepartment of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, P. R. China.
Yan-Xing ChenDepartment of Medical Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University, Guangzhou, 510060, P. R. China.
Hai-Yu MoDepartment of Medical Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University, Guangzhou, 510060, P. R. China.
Hui ShengDepartment of Medical Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University, Guangzhou, 510060, P. R. China.
Ze-Xian LiuDepartment of Medical Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University, Guangzhou, 510060, P. R. China.ORCID http://orcid.org/0000-0001-9698-0610
Zhao-Lei ZengDepartment of Medical Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University, Guangzhou, 510060, P. R. China.ORCID http://orcid.org/0000-0003-4420-5625
Xin-Yuan GuanDepartment of Clinical Oncology, Shenzhen Key Laboratory for Cancer Metastasis and Personalized Therapy, The University of Hong Kong-Shenzhen Hospital, Shenzhen, 518053, P. R. China.ORCID http://orcid.org/0000-0002-4485-6017
Huai-Qiang JuDepartment of Medical Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University, Guangzhou, 510060, P. R. China. juhq@sysucc.org.cn.ORCID http://orcid.org/0000-0003-1713-5465
Kun LiaoDepartment of Medical Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University, Guangzhou, 510060, P. R. China. liaokun@sysucc.org.cn.ORCID http://orcid.org/0000-0002-2949-8215
Rui-Hua XuDepartment of Medical Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University, Guangzhou, 510060, P. R. China. xurh@sysucc.org.cn.ORCID http://orcid.org/0000-0001-9771-8534

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82173128National Natural Science Foundation of China (National Science Foundation of China) 82303306
6 · The paper itself

Abstract

Despite advances in cancer immunotherapy, colorectal cancer patients exhibit limited therapeutic responses. Therefore, the exploration of strategies combining immunotherapy with adjuvant approaches to enhance adaptive immune responses is in demand. Here, we perform a customized in vivo CRISPR-Cas9 screen to target genes encoding membrane and secreted proteins in CRC mouse models with different immune characteristics. We observe that loss of membrane-bound transcription factor site-1 protease (MBTPS1) in tumor cells enhances antitumor immunity and potentiates anti-PD-1 therapy. Mechanistic studies reveal that tumor cell-intrinsic MBTPS1 competes with USP13 for binding to STAT1, thereby disrupting the USP13-dependent deubiquitination-mediated STAT1 stabilization. The upregulated STAT1-transcribed chemokines including CXCL9, CXCL10, and CXCL11, promote CXCR3

Indexed as

Colorectal NeoplasmsImmunotherapyProgrammed Cell Death 1 ReceptorAnimalsCD8-Positive T-LymphocytesCell Line, TumorCRISPR-Cas SystemsFemaleHumansImmune Checkpoint InhibitorsMiceMice, Inbred C57BLSTAT1 Transcription FactorImmune Checkpoint InhibitorsProgrammed Cell Death 1 ReceptorStat1 protein, mouseSTAT1 Transcription Factor

Identifiers

PMID40307212
PMCPMC12043911

What OpenQuestion 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 OpenQuestion graph.