Evidence map›Paper›PMID 41184620›Full record

ArticleActa pharmacologica Sinica2026

MS1-96 induces HIP1R-dependent PD-L1 degradation and promotes antitumor immunity in colorectal cancer.

Jin-Jin Peng, Min Shao, Yu-Yi Li, Jing Feng, Xin-Tian Zhang, Che Xu, Qing-Xin Xie, Wang-Shuang Chen, Jia-Qing Chen, Di Wu and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta pharmacologica Sinica, 2026. 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. Article
  2. Intracellular PD-L1: Functions, Regulation, and Therapeutic Implications.International journal of biological sciences · 2026
    Review
  3. 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

14 authors.

Jin-Jin Peng *Department of Gastroenterology, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200023, China.
Min Shao *Shanghai Frontiers Science Center of Targeted Drugs, School of Pharmaceutical Sciences, Shanghai Jiao Tong University, Shanghai, 200240, China.
Yu-Yi Li *Department of Gastroenterology, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200023, China.
Jing FengDepartment of Gastroenterology, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200023, China.
Xin-Tian ZhangDepartment of Gastroenterology, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200023, China.
Che XuDepartment of Gastroenterology, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200023, China.
Qing-Xin XieDepartment of Gastroenterology, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200023, China.
Wang-Shuang ChenDepartment of Gastroenterology, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200023, China.
Jia-Qing ChenDepartment of Gastroenterology, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200023, China.
Di WuDepartment of Gastroenterology, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200023, China.
Fang BaiShanghai Institute for Advanced Immunochemical Studies, ShanghaiTech University, Shanghai, 201210, China.
Han YaoDepartment of Gastroenterology, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200023, China. hanyao89@163.com.
Yu-Dao ShenShanghai Frontiers Science Center of Targeted Drugs, School of Pharmaceutical Sciences, Shanghai Jiao Tong University, Shanghai, 200240, China. yudao.shen@sjtu.edu.cn.
Xiang-Jun MengDepartment of Gastroenterology, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200023, China. xiangjunmeng@aliyun.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The programmed cell death protein 1 (PD-1)/programmed death-ligand 1 (PD-L1) pathway, a pivotal immune checkpoint, enables tumor immune evasion, and its blockade is fundamental to cancer immunotherapy. The development of small-molecule agents targeting the PD-1/PD-L1 pathway offers a promising strategy for enhancing antitumor immunity. In this study, we screened an in-house compound library using RKO cells to discover novel PD-L1 downregulators. MS1-96 was identified as a potent PD-L1 degrader that promotes lysosome-dependent PD-L1 degradation. Furthermore, MS1-96 effectively reduced PD-L1 protein levels across multiple colorectal cancer (CRC) cell lines. By disrupting the PD-1/PD-L1 pathway, MS1-96 enhances CD8

Indexed as

Antineoplastic AgentsB7-H1 AntigenColorectal NeoplasmsAnimalsCD8-Positive T-LymphocytesCell Line, TumorDNA-Binding ProteinsHumansLysosomesMiceMice, Inbred C57BLProteolysisAntineoplastic AgentsB7-H1 AntigenCD274 protein, humanDNA-Binding ProteinsHIP1 protein, humanantitumor immunitycolorectal cancerHIP1Rlysosomal degradationMS1-96PD-L1

Identifiers

PMID41184620
PMCPMC13018566

What OpenQuestion holds

Textmetadata
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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.