Evidence map›Paper›PMID 39256572›Full record

ArticleOncogene2024

USP33 facilitates the ovarian cancer progression via deubiquitinating and stabilizing CBX2.

Jiming Chen, Wulin Shan, Qiucheng Jia, Yao Chen, Wenjing Jiang, Yuan Tian, Xu Huang, Xiaoyu Li, Zengying Wang, Bairong Xia

Abstract read
PubMed Publisher
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 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

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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.

Jiming Chen *Department of Gynecology, The Affiliated Changzhou Second People's Hospital of Nanjing Medical University, Changzhou, Jiangsu, China.ORCID 0000-0002-0238-9158
Wulin Shan *Department of Obstetrics and Gynecology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.ORCID 0000-0002-0729-3315
Qiucheng Jia *Department of Gynecology, The Affiliated Changzhou Second People's Hospital of Nanjing Medical University, Changzhou, Jiangsu, China.
Yao Chen *Department of Obstetrics and Gynecology, Anhui Provincial Cancer Hospital, Hefei, Anhui, China.
Wenjing JiangDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.
Yuan TianDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.
Xu HuangDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.
Xiaoyu LiDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.
Zengying WangDepartment of Obstetrics and Gynecology, Anhui Provincial Cancer Hospital, Hefei, Anhui, China.
Bairong XiaDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China. xiabairong@ustc.edu.cn.ORCID 0009-0001-0494-7061

Funding

Heilongjiang Provincial Postdoctoral Science Foundation (Heilongjiang Postdoctoral Science Foundation) lbh-z18109National Natural Science Foundation of China (National Science Foundation of China) 81872430
6 · The paper itself

Abstract

Post-translational modifications of proteins play a pivotal role in both the initiation and progression of ovarian cancer. Despite the recognition of USP33 as a significant factor in various cancers, its specific function and underlying mechanisms in ovarian cancer remain elusive. Proteomics and ubiquitinomics approaches were coupled to screen novel substrate proteins directly regulated by USP33. Our findings unveil that USP33 was observed to eliminate K27- and K48-linked ubiquitin chains from CBX2 at the K277 position. Notably, acetylation of CBX2 at K199, catalyzed by lysine acetyltransferase GCN5, was found to enhance its interaction with USP33, subsequently promoting further deubiquitination and stabilization. Functionally, our experiments demonstrate that USP33 significantly enhances ovarian cancer proliferation and metastasis in a CBX2-dependent manner. Furthermore, analysis revealed a direct positive correlation between the expression levels of USP33 and CBX2 proteins in human specimens, with elevated levels being associated with reduced survival rates in ovarian cancer patients. These findings elucidate the mechanism by which USP33 augments ovarian cancer progression through the stabilization of CBX2, underscoring the USP33-CBX2 axis as a promising therapeutic target in ovarian cancer management.

Indexed as

Disease ProgressionOvarian NeoplasmsPolycomb Repressive Complex 1UbiquitinationAnimalsCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMiceProtein StabilityUbiquitin ThiolesteraseCBX2 protein, humanPolycomb Repressive Complex 1Ubiquitin ThiolesteraseUSP33 protein, human

Identifiers

PMID39256572

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Registered trials

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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.