Evidence map›Paper›PMID 35414775›Full record

ArticleInternational journal of biological sciences2022

A SIX1 degradation inducer blocks excessive proliferation of prostate cancer.

Yuning Liao, Wenshuang Sun, Zhenlong Shao, Yuan Liu, Xiaoyu Zhong, Yuanfei Deng, Fang Liu, Hongbiao Huang, Jinbao Liu

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

13 citing papers in PubMed, 23 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

9 authors at 3 institutions in 1 country.

Yuning LiaoAffiliated Cancer Hospital & institute of Guangzhou Medical University, Guangzhou, Guangdong, 510095, China.
Wenshuang SunGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China.
Zhenlong ShaoGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China.
Yuan LiuGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China.
Xiaoyu ZhongGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China.
Yuanfei DengDepartment of Pathology, First People's Hospital of Foshan, 528000 Foshan, Guangdong, China.
Fang LiuDepartment of Pathology, First People's Hospital of Foshan, 528000 Foshan, Guangdong, China.
Hongbiao HuangAffiliated Cancer Hospital & institute of Guangzhou Medical University, Guangzhou, Guangdong, 510095, China.
Jinbao LiuAffiliated Cancer Hospital & institute of Guangzhou Medical University, Guangzhou, Guangdong, 510095, China.
Guangzhou Medical University · CNGuangzhou Medical University Cancer Hospital · CNFirst People's Hospital of Foshan · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer (PC) remains a great medical challenge due to its high incidence and the development of castration resistance in patients treated with androgen deprivation therapy. Deubiquitinases, the enzymes that specifically hydrolyze ubiquitin chains on their substrates, were recently proposed as a serious of critical therapeutic targets for cancer treatment. Our previous study has been reported that the ubiquitin specific peptidase 1 (USP1) functionally acts as a deubiquitinase of sine oculis homeobox homolog 1 (SIX1) and contributes to the proliferation and castration resistance of PC. The stabilization of SIX1 by USP1 partially depends on the status of glucose-regulated protein 75 (GRP75). In this study, we aimed to identify a SIX1 degradation inducer via inhibiting the USP1-SIX1 axis. we screened a range of kinase inhibitors and showed that SNS-032 is the best candidate to trigger the ubiquitinated degradation of SIX1. SNS-032 not only restrains activity of the USP1-SIX1 axis and cell cycle progression, but also results in apoptosis of PC cells. Moreover, the combination of SNS-032 and enzalutamide synergistically induces apoptosis and downregulates expression of USP1, SIX1, and AR/AR-V7 in AR-V7 highly expressed 22Rv1 cells. Overall, our findings may develop a novel and effective strategy to overcome castration resistance in PC for the identification of a SIX1 degradation inducer via targeting the USP1-SIX1 axis.

Indexed as

Androgen AntagonistsProstatic Neoplasms, Castration-ResistantCell Line, TumorCell ProliferationHomeodomain ProteinsHumansMaleReceptors, AndrogenAndrogen AntagonistsHomeodomain ProteinsReceptors, AndrogenSIX1 protein, humanDegradationProstate cancerSIX1SNS-032USP1

Identifiers

PMID35414775
PMCPMC8990483
OpenAlexW4225766250

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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.