Evidence map›Paper›PMID 39112516›Full record

ArticleOncogene2024

A noncanonical E3 ubiquitin ligase RNF41-mediated MYO1C stability promotes prostate cancer metastasis by inducing actin remodeling.

Situ Xiong, Sheng Li, Zhongqi Li, Yanping Song, Lin Yang, Hailang Yang, Jing Xiong, Wang Pan, Ju Guo, Bin Fu and 1 more

Abstract read
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In one paragraph

Article in Oncogene, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
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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

11 authors.

Situ Xiong *Jiangxi Provincial Key Laboratory of Urinary System Diseases, Department of Urology, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Sheng Li *Jiangxi Provincial Key Laboratory of Urinary System Diseases, Department of Urology, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Zhongqi LiJiangxi Provincial Key Laboratory of Urinary System Diseases, Department of Urology, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Yanping SongDepartment of Quality Control, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Lin YangJiangxi Provincial Key Laboratory of Urinary System Diseases, Department of Urology, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Hailang YangJiangxi Provincial Key Laboratory of Urinary System Diseases, Department of Urology, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Jing XiongJiangxi Provincial Key Laboratory of Urinary System Diseases, Department of Urology, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Wang PanCollege of Chemical and Environmental Engineering, Shanghai Institute of Technology, Shanghai, China.
Ju GuoJiangxi Provincial Key Laboratory of Urinary System Diseases, Department of Urology, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China. 544949441@qq.com.
Bin FuJiangxi Provincial Key Laboratory of Urinary System Diseases, Department of Urology, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China. ndyfy02157@ncu.edu.cn.
Songhui XuJiangxi Provincial Key Laboratory of Urinary System Diseases, Department of Urology, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China. ndyfy10021@ncu.edu.cn.ORCID 0000-0003-0269-9129

Funding

National Natural Science Foundation of China (National Science Foundation of China) Grant no. 20151BAB205047National Natural Science Foundation of China (National Science Foundation of China) Grant No. 82172921National Natural Science Foundation of China (National Science Foundation of China) Grant No. 82260500
6 · The paper itself

Abstract

Prostate cancer bone metastasis is a predominant cause of death for prostate cancer (PCa) patients. However, the underlying mechanisms are poorly understood. Here, we report that high levels of RNF41 are associated with metastatic human prostate cancer. RNF41 silencing inhibits prostate cancer cell growth, cell migration and invasion in vitro and in vivo. Mechanistically, we identify that RNF41 induces K27- and K63-linked noncanonical polyubiquitination of MYO1C to enhance its stability and induce actin remodeling, which promotes PCa bone metastasis. RNF41 was significantly upregulated in metastatic prostate cancer tissues and positively associated with MYO1C expression. Furthermore, we show in intraarterial injected-bone metastasis xenograft model that targeting MYO1C stability by inhibition of RNF41 markedly suppressed PCa bone metastasis. Collectively, our findings identify RNF41 is an important regulator of prostate cancer cell growth and metastasis and targeting RNF41/MYO1C could be a valuable strategy to ameliorate prostate cancer progression and metastasis.

Indexed as

Bone NeoplasmsMyosin Type IProstatic NeoplasmsUbiquitin-Protein LigasesActinsAnimalsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsMaleMiceNeoplasm MetastasisProtein StabilityActinsIntracellular Signaling Peptides and ProteinsMYO1C protein, humanMyosin Type IRNF14 protein, humanRNF41 protein, humanUbiquitin-Protein Ligases

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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.