Evidence map›Paper›PMID 32719332›Full record

ArticleCell death & disease2020

Stabilization of ADAM9 by N-α-acetyltransferase 10 protein contributes to promoting progression of androgen-independent prostate cancer.

Yung-Wei Lin, Yu-Ching Wen, Chih-Ying Chu, Min-Che Tung, Yi-Chieh Yang, Kuo-Tai Hua, Ke-Fan Pan, Michael Hsiao, Wei-Jiunn Lee, Ming-Hsien Chien

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
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  7. Potential Influence ofInternational journal of molecular sciences · 2025
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  11. Conformational plasticity links structural instability of NAA10Computational and structural biotechnology journal · 2024
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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 6 institutions in 1 country.

Yung-Wei LinDepartment of Urology, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan.
Yu-Ching WenDepartment of Urology, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan.
Chih-Ying ChuGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Min-Che TungGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Yi-Chieh YangGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Kuo-Tai HuaGraduate Institute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Ke-Fan PanGraduate Institute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Michael HsiaoGenomics Research Center, Academia Sinica, Taipei, Taiwan.ORCID http://orcid.org/0000-0001-8529-9213
Wei-Jiunn LeeTMU Research Center of Urology and Kidney (TMU-RCUK), Taipei Medical University, Taipei, Taiwan. lwj5905@gmail.com.
Ming-Hsien ChienGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan. mhchien1976@gmail.com.ORCID http://orcid.org/0000-0002-0084-7231
National Taiwan University · TWTaipei Medical University Hospital · TWTungs' Taichung MetroHarbor Hospital · TWWan Fang Hospital · TWGenomics Research Center, Academia Sinica · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

N-α-Acetyltransferase 10 protein (Naa10p) was reported to be an oncoprotein in androgen-dependent prostate cancer (PCa; ADPC) through binding and increasing transcriptional activity of the androgen receptor (AR). PCa usually progresses from an androgen-dependent to an androgen-independent stage, leading to an increase in the metastatic potential and an incurable malignancy. At present, the role of Naa10p in androgen-independent prostate cancer (AIPC) remains unclear. In this study, in silico and immunohistochemistry analyses showed that Naa10 transcripts or the Naa10p protein were more highly expressed in primary and metastatic PCa cancer tissues compared to adjacent normal tissues and non-metastatic cancer tissues, respectively. Knockdown and overexpression of Naa10p in AIPC cells (DU145 and PC-3M), respectively, led to decreased and increased cell clonogenic and invasive abilities in vitro as well as tumor growth and metastasis in AIPC xenografts. From the protease array screening, we identified a disintegrin and metalloprotease 9 (ADAM9) as a potential target of Naa10p, which was responsible for the Naa10p-induced invasion of AIPC cells. Naa10p can form a complex with ADAM9 to maintain ADAM9 protein stability and promote AIPC's invasive ability which were independent of its acetyltransferase activity. In contrast to the Naa10p-ADAM9 axis, ADAM9 exerted positive feedback regulation on Naa10p to modulate progression of AIPC in vitro and in vivo. Taken together, for the first time, our results reveal a novel cross-talk between Naa10p and ADAM9 in regulating the progression of AIPC. Disruption of Naa10p-ADAM9 interactions may be a potential intervention for AIPC therapy.

Indexed as

ADAM ProteinsAndrogensAnimalsCarcinogenesisCastrationCell Line, TumorCell ProliferationClone CellsDisease Models, AnimalDisease ProgressionFeedback, PhysiologicalGene Expression Regulation, NeoplasticHumansMaleMembrane ProteinsMice, SCIDADAM9 protein, humanADAM ProteinsAndrogensMembrane ProteinsNAA10 protein, humanN-Terminal Acetyltransferase AN-Terminal Acetyltransferase E

Identifiers

PMID32719332
PMCPMC7385149
OpenAlexW3045175585

What OpenQuestion holds

Textmetadata
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.