Evidence map›Paper›PMID 39538297›Full record

ArticleBiomarker research2024

Exosomal PSM-E inhibits macrophage M2 polarization to suppress prostate cancer metastasis through the RACK1 signaling axis.

Xingliang Qin, Ruoxi Niu, Yongyao Tan, Yuxin Huang, Weishu Ren, Weiwei Zhou, Huiquan Wu, Junlong Zhang, Mingze Xu, Xiang Zhou and 4 more

Erratum issuedAbstract read
In one paragraph

Article in Biomarker research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors.

Xingliang Qin *Department of Endocrinology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.
Ruoxi Niu *School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, 999077, China.
Yongyao Tan *Key Laboratory of Tropical Disease Control (Sun Yat-sen University), Ministry of Education, Guangzhou, 510080, China.
Yuxin Huang *Department of Urology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.
Weishu RenKey Laboratory of Tropical Disease Control (Sun Yat-sen University), Ministry of Education, Guangzhou, 510080, China.
Weiwei ZhouKey Laboratory of Tropical Disease Control (Sun Yat-sen University), Ministry of Education, Guangzhou, 510080, China.
Huiquan WuGuangzhou Jishiyuan Bio-technology Co., Ltd., Guangzhou, 510700, China.
Junlong ZhangDepartment of Urology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.
Mingze XuDepartment of Urology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.
Xiang ZhouDepartment of Microsurgery, Trauma and Hand Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China.
Hongyu GuanDepartment of Endocrinology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.
Xun ZhuKey Laboratory of Tropical Disease Control (Sun Yat-sen University), Ministry of Education, Guangzhou, 510080, China. zhuxun8@mail.sysu.edu.cn.
Yu ChenDepartment of Urology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China. chenyu8@mail.sysu.edu.cn.
Kaiyuan CaoKey Laboratory of Tropical Disease Control (Sun Yat-sen University), Ministry of Education, Guangzhou, 510080, China. caoky@mail.sysu.edu.cn.

Funding

Guangdong Basic and Applied Basic Research Foundation 2021A1515010597the National Natural Science Foundation of China 82071352, 82341094, 82171675, 81672556
6 · The paper itself

Abstract

backgroundIt is well-established that understanding the mechanism of prostate cancer (PCa)-associated metastasis is paramount for improving its prognosis. Metastasis is known to involve the communication between tumor-associated macrophages (TAMs) and tumor cells. Exosomes are crucial in mediating this intercellular communication within the tumor microenvironment. Nonetheless, the role of exosomal proteins in PCa metastasis is not yet fully understood. Here, we investigated the mechanisms of prostate cancer-derived exosomal PSM-E on regulating macrophage M2 polarization to suppress tumor invasion and metastasis.

methodsPSM-E levels in exosomes were detected by transmission electron microscopy and Western blotting analysis. The diagnostic value of urine-derived exosomal PSM-E in PCa were evaluated by LC-MS/MS, correlation analysis, and ROC curves analysis. The mechanisms underlying the inhibitory effect of exosomal PSM-E on the M2 polarization of macrophages was investigated by co-IP, IHC staining, and PCa tumorigenesis model, etc.

resultsWe revealed that exosomal PSM-E is upregulated in exosomes derived from the serum and urine of PCa patients. Clinically, an elevated exosomal PSM-E expression in urine is significantly correlated with an advanced pathological tumor stage and a high Gleason score. Our research also revealed that exosomal PSM-E inhibits prostate cancer cell proliferation, invasion, and metastasis by suppressing macrophage polarization in vitro and in vivo. Furthermore, we provided compelling evidence that exosomal PSM-E inhibits M2 polarization of macrophages by recruiting RACK1 and suppressing the FAK and ERK signaling pathways, consequently suppressing PCa invasion and metastasis. Furthermore, we found that the protease-associated domain of PSM-E and the fourth tryptophan-aspartate repeat of RACK1 are crucial for the interaction between PSM-E and RACK1.

conclusionsNotably, exosomes carrying PSM-E from PCa urine could potentially serve as a biomarker for PCa, and targeting exosomal PSM-E may represent a strategy for preventing tumor progression in this patient population.

Indexed as

ExosomeMacrophage polarizationProstate cancerPSM-E

Identifiers

PMID39538297
PMCPMC11562865

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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.