Evidence map›Paper›PMID 34584067›Full record

ArticleCell death & disease2021

USP28 facilitates pancreatic cancer progression through activation of Wnt/β-catenin pathway via stabilising FOXM1.

Leifeng Chen, Zheng Xu, Qing Li, Qian Feng, Cihua Zheng, Yunyan Du, Rongfa Yuan, Xiaogang Peng

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 65 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

8 authors at 1 institution in 1 country.

Leifeng Chen *Department of General Surgery, the Second Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi Province, China.ORCID 0000-0001-8305-1900
Zheng Xu *Department of General Surgery, the Second Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi Province, China.
Qing Li *Department of Pathology, the Second Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi Province, China.
Qian FengDepartment of General Surgery, the Second Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi Province, China.
Cihua ZhengDepartment of General Surgery, the Second Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi Province, China.
Yunyan DuDepartment of Medical, Jiangxi Provincial People's Hospital of Nanchang University, Nanchang, 330006, China. 342327252@qq.com.ORCID 0000-0002-2448-9520
Rongfa YuanDepartment of General Surgery, the Second Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi Province, China. pxg8205@163.com.ORCID 0000-0001-8204-0839
Xiaogang PengJiangxi Province Key Laboratory of Molecular Medicine, the Second Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi Province, China. pxg8205@163.com.ORCID 0000-0002-8173-5118
Nanchang University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81560117
6 · The paper itself

Abstract

Ubiquitination is an important post-translational modification that can be reversed by a family of enzymes called deubiquitinating enzymes (DUBs). Ubiquitin-specific protease 28 (USP28), a member of the DUBs family, functions as a potential tumour promoter in various cancers. However, the biological function and clinical significance of USP28 in pancreatic cancer (PC) are still unclear. Here, we showed that PC tumours had higher USP28 expression compared with that of normal pancreatic tissues, and high USP28 level was significantly correlated with malignant phenotype and shorter survival in patients with PC. Overexpression of USP28 accelerated PC cell growth, whereas USP28 knockdown impaired PC cell growth both in vitro and in vivo. Further, we found that USP28 promoted PC cell growth by facilitating cell cycle progression and inhibiting apoptosis. Mechanistically, USP28 deubiquitinated and stabilised FOXM1, a critical mediator of Wnt/β-catenin signalling. USP28-mediated stabilisation of FOXM1 significantly promoted nucleus β-catenin trans-activation, which in turn led to the activation of the Wnt/β-catenin pathway. Finally, restoration of FOXM1 expression abolished the anti-tumour effects of USP28-silencing. Thus, USP28 contributes to PC pathogenesis through enhancing the FOXM1-mediated Wnt/β-catenin signalling, and could be a potential diagnostic and therapeutic target for PC cases.

Indexed as

Disease ProgressionWnt Signaling PathwayAgedAnimalsApoptosisCarcinogenesisCell CycleCell Line, TumorCell ProliferationFemaleForkhead Box Protein M1Gene Expression Regulation, NeoplasticHumansMaleMiceMice, Inbred BALB CForkhead Box Protein M1FOXM1 protein, humanRNA, MessengerUbiquitin ThiolesteraseUSP28 protein, human

Identifiers

PMID34584067
PMCPMC8478945
OpenAlexW3204423549

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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.