Evidence map›Paper›PMID 39227807›Full record

ArticleCell communication and signaling : CCS2024

NDR1 mediates PD-L1 deubiquitination to promote prostate cancer immune escape via USP10.

Meiling Fu, Jinxin Li, Zuodong Xuan, Zeyuan Zheng, Yankuo Liu, Zeyi Zhang, Jianzhong Zheng, Min Zhong, Bin Liu, Yifan Du and 2 more

Abstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

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  17. Ubiquitin-Specific Protease 10: A New Target in Tumor Immune Escape.Cancer control : journal of the Moffitt Cancer Center
    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

12 authors.

Meiling Fu *Department of Urology, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361101, China.
Jinxin Li *Department of Urology, Changhai Hospital, Naval Medical University (Second Military Medical University), Shanghai, China.
Zuodong Xuan *Department of Urology, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361101, China.
Zeyuan ZhengDepartment of Urology, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361101, China.
Yankuo LiuDepartment of Urology, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361101, China.
Zeyi ZhangDepartment of Urology, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361101, China.
Jianzhong ZhengDepartment of Urology, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361101, China.
Min ZhongDepartment of Urology, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361101, China.
Bin LiuDepartment of Urology, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361101, China.
Yifan DuDepartment of Urology, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361101, China.
Lei ZhangSchool of Public Health, Xiamen University, Xiamen, 361101, China. Drzhanglei@xmu.edu.cn.
Huimin SunDepartment of Urology, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361101, China. hmsun@xah.xmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer (PCa) is one of the most common male genitourinary system malignancies. Despite the significant benefits of anti-PD-L1 immune checkpoint inhibitor therapy in other cancers, the reasons for its poor therapeutic efficacy in prostate cancer (PCa) remain unclear.NDR1 plays an important role in innate immunity, but its role in tumor immunity and immunotherapy has not been investigated. The role of NDR1 in the immune microenvironment of PCa and the related mechanisms are unknown. Here, we found a positive correlation between NDR1 and PD-L1 expression in PCa. NDR1 significantly inhibits CD8 + T cell infiltration and function, thereby promoting immune escape in prostate cancer.More importantly, NDR1 inhibition significantly enhanced CD8 + T cell activation, which enhanced the therapeutic effect of anti-PD-L1. Mechanistic studies revealed that NDR1 inhibits ubiquitination-mediated PD-L1 degradation via the deubiquitinase USP10, upregulates PD-L1, and promotes PCa immune escape. Thus, our study suggests a unique PD-L1 regulatory mechanism underlying PCa immunotherapy failure. The significance of NDR1 in PCa immune escape and its mechanism of action were clarified, and combined NDR1/PD-L1 inhibition was suggested as an approach to boost PCa immunotherapy effectiveness.

Indexed as

B7-H1 AntigenProstatic NeoplasmsTumor EscapeUbiquitinationUbiquitin ThiolesteraseAnimalsCD8-Positive T-LymphocytesCell Line, TumorHumansMaleMiceTumor MicroenvironmentB7-H1 AntigenCD274 protein, humanUbiquitin ThiolesteraseUSP10 protein, humanAnti-PD-1 therapyImmune checkpoint BlockadeImmune escapeNDR1/STK38, PD-L1Prostate cancer

Identifiers

PMID39227807
PMCPMC11370014

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.