Evidence map›Paper›PMID 39149855›Full record

ArticleCancer medicine2024

The miRNAs 203a/210-3p/5001-5p regulate the androgen/androgen receptor/YAP-induced migration in prostate cancer cells.

Chieh Huo, Ying-Yu Kuo, Ching-Yu Lin, Shine-Gwo Shiah, Chia-Yang Li, Shu-Pin Huang, Jen-Kun Chen, Wen-Ching Wang, Hsing-Jien Kung, Chih-Pin Chuu

Abstract read
In one paragraph

Article in Cancer medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

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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

4 citing papers in PubMed.

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4 · The record

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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.

Chieh HuoInstitute of Cellular and System Medicine, National Health Research Institutes, Zhunan, Taiwan.
Ying-Yu KuoInstitute of Cellular and System Medicine, National Health Research Institutes, Zhunan, Taiwan.
Ching-Yu LinInstitute of Cellular and System Medicine, National Health Research Institutes, Zhunan, Taiwan.
Shine-Gwo ShiahNational Institute of Cancer Research, National Health Research Institutes, Zhunan, Taiwan.
Chia-Yang LiGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Shu-Pin HuangDepartment of Urology, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Jen-Kun ChenInstitute of Biomedical Engineering and Nanomedicine, National Health Research Institutes, Zhunan, Taiwan.
Wen-Ching WangInstitute of Molecular and Cellular Biology, National Tsing Hua University, Hsinchu, Taiwan.
Hsing-Jien KungPh.D. Program for Cancer Molecular Biology and Drug Discovery, Taipei Medical University, Taipei, Taiwan.
Chih-Pin ChuuInstitute of Cellular and System Medicine, National Health Research Institutes, Zhunan, Taiwan.ORCID 0000-0001-7206-7923

Funding

Ministry of Science and Technology, Taiwan MOST 105-2628-B-400-005-MY3; MOST 109-2320-B-400-0National Health Research Institutes NHRIKMU-111-I002; CS-109-PP-03; CS-112-PP-03; CS-1National Science and Technology Council NSTC 112-2314-B-400-031; NSTC 112-2320-B-400-008NSTC 112-2326-B-038-001
6 · The paper itself

Abstract

backgroundProstate cancer (PCa) patients with elevated level of androgen receptor (AR) correlate with higher metastatic incidence. Protein expression of AR and its target gene prostate-specific antigen (PSA) are elevated in metastatic prostate tumors as compared to organ-confined tumors. Androgen treatment or elevation of AR promotes metastasis of PCa in cell culture and murine model. However, under androgen depleted condition, AR suppressed cell mobility and invasiveness of PCa cells. Androgen deprivation therapy in PCa patients is associated with higher risk of cancer metastasis. We therefore investigated the dual roles of AR and miRNAs on PCa metastasis.

methodsThe PC-3

resultsIn the absence of androgen, AR repressed the migration and invasion of PCa cells. When androgen was present, AR stimulated the migration and invasion of PCa cells both in vitro and in zebrafish xenotransplantation model. Androgen increased phospho-AR Ser81 and yes-associated protein 1 (YAP), decreased phospho-YAP Ser217, and altered epithelial-mesenchymal transition (EMT) proteins in PCa cells. Co-IP assay demonstrated that androgen augmented the interaction between YAP and AR in nucleus. Knockdown of YAP or treatment with YAP inhibitor abolished the androgen-induced migration and invasion of PCa cells, while overexpression of YAP showed opposite effects. The miRNA array revealed that androgen decreased hsa-miR-5001-5p but increased hsa-miR-203a and hsa-miR-210-3p in PC-3AR cells but not PC-3 cells. Treatment with inhibitors targeting hsa-miR-203a/hsa-miR-210-3p, or overexpression of hsa-miR-5001-5p decreased YAP expression as well as suppressed the androgen-induced migration and invasion of PCa cells. Chromatin immunoprecipitation (ChIP) assay demonstrated that AR binds with promoter region of has-miR-210-3p in the presence of androgen.

conclusionsOur observations indicated that miRNAs 203a/210-3p/5001-5p regulate the androgen/AR/YAP-induced PCa metastasis.

Indexed as

Cell MovementGene Expression Regulation, NeoplasticMicroRNAsProstatic NeoplasmsReceptors, AndrogenTranscription FactorsYAP-Signaling ProteinsZebrafishAdaptor Proteins, Signal TransducingAndrogensAnimalsCell Line, TumorHumansMaleMiceZebrafish ProteinsAdaptor Proteins, Signal TransducingAndrogensAR protein, humanMicroRNAsReceptors, AndrogenTranscription FactorsYAP1 protein, humanYAP-Signaling ProteinsYes-associated protein (yap), zebrafishZebrafish ProteinsandrogenARmiRNAprostate cancer metastasisYAP

Identifiers

PMID39149855
PMCPMC11327718

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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.