Evidence map›Paper›PMID 37501397›Full record

ArticleCancer medicine2023

Prostate cancer cells synergistically defend against CD8

Dameng Li, Xueying Zhou, Wenxian Xu, Yuxin Chen, Chenglong Mu, Xinchun Zhao, Tao Yang, Gang Wang, Liang Wei, Bo Ma

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.2field-weighted citation impact, top 5% of its field
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

27 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
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  11. Bolstering CD8Biology · 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

10 authors at 2 institutions in 1 country.

Dameng LiCancer Institute, Xuzhou Medical University, Xuzhou, China.
Xueying ZhouCancer Institute, Xuzhou Medical University, Xuzhou, China.
Wenxian XuCancer Institute, Xuzhou Medical University, Xuzhou, China.
Yuxin ChenCancer Institute, Xuzhou Medical University, Xuzhou, China.
Chenglong MuCancer Institute, Xuzhou Medical University, Xuzhou, China.
Xinchun ZhaoCancer Institute, Xuzhou Medical University, Xuzhou, China.
Tao YangCancer Institute, Xuzhou Medical University, Xuzhou, China.
Gang WangCancer Institute, Xuzhou Medical University, Xuzhou, China.
Liang WeiCancer Institute, Xuzhou Medical University, Xuzhou, China.
Bo MaCancer Institute, Xuzhou Medical University, Xuzhou, China.ORCID 0000-0003-0816-6630
Jiangsu University · CNXuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMetastatic castration-resistant prostate cancer (mCRPC) remains fatal and incurable, despite a variety of treatments that can delay disease progression and prolong life. Immune checkpoint therapy is a promising treatment. However, emerging evidence suggests that exosomal programmed necrosis ligand 1 (PD-L1) directly binds to PD-1 on the surface of T cells in the drain lineage lymph nodes or neutralizes administered PD-L1 antibodies, resulting in poor response to anti-PD-L1 therapy in mCRPC. MATERIALS AND

methodsWestern blotting and immunofluorescence were performed to compare PD-L1 levels in exosomes derived from different prostate cancer cells. PC3 cells were subcutaneously injected into nude mice, and then ELISA assay was used to detect human specific PD-L1 in exosomes purified from mouse serum. The function of CD8

resultsHerein, we found that exosomal-PD-L1 was taken up by tumor cells expressing low levels of PD-L1, thereby protecting them from T-cell killing. Higher levels of PD-L1 were detected in exosomes derived from the highly malignant prostate cancer PC3 and DU145 cell lines. Moreover, exosomal PD-L1 was taken up by the PD-L1-low-expressing LNCaP cell line and inhibited the killing function of CD8-T cells on tumor cells. The growth rate of RM1-derived subcutaneous tumors was decreased after knockdown of PD-L1 in tumor cells, whereas the growth rate recovered following exosomal PD-L1 tail vein injection. Furthermore, in the serum of mice with PCa subcutaneous tumors, PD-L1 was mainly present on exosomes.

conclusionIn summary, tumor cells share PD-L1 synergistically against T cells through exosomes. Inhibition of exosome secretion or prevention of PD-L1 sorting into exosomes may improve the therapeutic response of prostate tumors to anti-PD-L1 therapy.

Indexed as

ExosomesProstatic Neoplasms, Castration-ResistantAnimalsB7-H1 AntigenCD8-Positive T-LymphocytesCell Line, TumorDisease ProgressionHumansMaleMiceMice, NudeB7-H1 Antigenanti-PD-L1 therapyCD8+ T cellsexosomesPD-L1prostate cancer

Identifiers

PMID37501397
PMCPMC10469662
OpenAlexW4385330596

What OpenQuestion holds

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LicenceCC BY
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.