Evidence map›Paper›PMID 38415977›Full record

ArticleImmunity, inflammation and disease2024

Knockdown of liver cancer cell-secreted exosomal PSMA5 controls macrophage polarization to restrain cancer progression by blocking JAK2/STAT3 signaling.

Shujie Xie, Xiang Li, Jia Yan, Hua Yu, Shuhuai Chen, Kana Chen

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

Article in Immunity, inflammation and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 13 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Shujie XieDepartment of Hepatobiliary and Pancreatic Surgery, Ningbo No.2 Hospital, Ningbo, Zhejiang, China.
Xiang LiDepartment of Hepatobiliary and Pancreatic Surgery, Ningbo No.2 Hospital, Ningbo, Zhejiang, China.
Jia YanDepartment of Hepatobiliary and Pancreatic Surgery, Ningbo No.2 Hospital, Ningbo, Zhejiang, China.
Hua YuDepartment of Hepatobiliary and Pancreatic Surgery, Ningbo No.2 Hospital, Ningbo, Zhejiang, China.
Shuhuai ChenDepartment of Hepatobiliary and Pancreatic Surgery, Ningbo No.2 Hospital, Ningbo, Zhejiang, China.
Kana ChenDepartment of Plastic Surgery, Ningbo No.2 Hospital, Ningbo, Zhejiang, China.ORCID http://orcid.org/0000-0002-3985-6354
Ningbo No. 2 Hospital · CN

Funding

Huamei Foundation of University of Chinese Academy of Sciences 2018HMKY03Huamei Foundation of University of Chinese Academy of Sciences 2019HMKY30Huamei Foundation of University of Chinese Academy of Sciences 2021HMKY16Ningbo Medical Science and Technology Programme 2018A67Ningbo Natural Science Foundation 2021J316
6 · The paper itself

Abstract

introductionTumor-associated macrophages, a major component of the tumor microenvironment, undergo polarization into M2 macrophages (M2), and thereby exert an immunosuppressive effect to induce cancer metastasis. This study strives to uncover a molecular mechanism underlying this event in hepatocellular carcinoma (HCC).

methodsProteasome subunit alpha 5 (PSMA5) expression in liver hepatocellular carcinoma (LIHC) tissues and its association with LIHC patients were predicted using StarBase. PSMA5 level in human HCC cells was manipulated via transfection. Exosomes were isolated from HCC cells, and internalized into macrophages which were cocultured with HCC cells. Exosome internalization was observed after fluorescence labeling. HCC cell migration and invasion were evaluated by wound healing and Transwell assays. Xenograft assay was performed to investigate the role of PSMA5 in in vitro tumorigenesis. M2 polarization was assessed by enzyme-linked immunosorbent assay, quantitative reverse transcription polymerase chain reaction, and immunohistochemistry. PSMA5 expression in exosomes and Janus Kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) activation in macrophages and tumors were detected by Western blot analysis.

resultsHigh PSMA5 expression was observed in LIHC tissues and associated with compromised survival of LIHC patients. PSMA5 knockdown inhibited HCC cell migration and invasion. PSMA5 knockdown in HCC cells downregulated PSMA5 level in exosomes from these HCC cells. HCC cell-isolated exosomes were successfully internalized into macrophages, and facilitated M2 polarization and JAK2/STAT3 pathway activation. HCC cell-secreted exosomal PSMA5 knockdown inhibited the exosome-induced effect on macrophages, and attenuated the promotion induced by exosome-treated macrophages on HCC cell migration/invasion and tumorigenesis along with in vivo M2 polarization and JAK2/STAT3 pathway activation.

conclusionHCC cell-secreted exosomal PSMA5 knockdown hinders M2 polarization to suppress cancer progression by restraining JAK2/STAT3 signaling.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsCarcinogenesisHumansJanus Kinase 2Proteasome Endopeptidase ComplexSTAT3 Transcription FactorTumor MicroenvironmentJAK2 protein, humanJanus Kinase 2Proteasome Endopeptidase ComplexPSMA5 protein, humanSTAT3 protein, humanSTAT3 Transcription Factorexosomeshepatocellular carcinomaJAK2/STAT3 signalingM2 macrophagePSMA5

Identifiers

PMID38415977
PMCPMC10836037
OpenAlexW4391474003

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.