Evidence map›Paper›PMID 38953362›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

Targeting Nuclear Receptor Coactivator SRC-1 Prevents Colorectal Cancer Immune Escape by Reducing Transcription and Protein Stability of PD-L1.

Yilin Hong, Qiang Chen, Zinan Wang, Yong Zhang, Bei Li, Hanshi Guo, Chuanzhong Huang, Xu Kong, Pingli Mo, Nengming Xiao and 3 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

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  16. ID3 enhances PD-L1 expression by restructuring MYC to promote colorectal cancer immune evasion.Proceedings of the National Academy of Sciences of the United States of America · 2025
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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.

Yilin HongState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, 361102, P. R. China.
Qiang ChenZhejiang Key Laboratory of Pathophysiology, Department of Biochemistry and Molecular Biology, Health Science Center, Ningbo University, Ningbo, Zhejiang, 315211, P. R. China.
Zinan WangState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, 361102, P. R. China.
Yong ZhangState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, 361102, P. R. China.
Bei LiState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, 361102, P. R. China.
Hanshi GuoState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, 361102, P. R. China.
Chuanzhong HuangLaboratory of Immuno-Oncology, Clinical Oncology School of Fujian Medical University, Fujian Cancer Hospital, Fuzhou, 350014, P. R. China.
Xu KongCancer Research Center, School of Medicine, Xiamen University, Xiamen, 361102, P. R. China.
Pingli MoState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, 361102, P. R. China.
Nengming XiaoState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, 361102, P. R. China.
Jianming XuDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, 77030, USA.
Yunbin YeLaboratory of Immuno-Oncology, Clinical Oncology School of Fujian Medical University, Fujian Cancer Hospital, Fuzhou, 350014, P. R. China.
Chundong YuState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, 361102, P. R. China.ORCID 0000-0002-4141-8345

Funding

Key Laboratory of Precision Medicine for Atherosclerotic Diseases of Zhejiang Province, China 2022E10026National Natural Science Foundation of China 82173086National Natural Science Foundation of China 82303144Natural Science Foundation of Ningbo Municipality 2023J375Zhejiang Provincial Natural Science Foundation of China LQ24H160002
6 · The paper itself

Abstract

Programmed death-ligand 1 (PD-L1) is overexpressed in multiple cancers and critical for their immune escape. It has previously shown that the nuclear coactivator SRC-1 promoted colorectal cancer (CRC) progression by enhancing CRC cell viability, yet its role in CRC immune escape is unclear. Here, we demonstrate that SRC-1 is positively correlated with PD-L1 in human CRC specimens. SRC-1 deficiency significantly inhibits PD-L1 expression in CRC cells and retards murine CRC growth in subcutaneous grafts by enhancing CRC immune escape via increasing tumor infiltration of CD8

Indexed as

B7-H1 AntigenColorectal NeoplasmsDisease Models, AnimalNuclear Receptor Coactivator 1Tumor EscapeAnimalsCell Line, TumorHumansMiceMice, Inbred C57BLProtein StabilityB7-H1 AntigenCD274 protein, humanNuclear Receptor Coactivator 1colorectal cancerimmune escapeimmunotherapyPD‐L1SRC‐1

Identifiers

PMID38953362
PMCPMC11434141

What OpenQuestion holds

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Registered trials

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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.