Evidence map›Paper›PMID 35383144›Full record

ArticleCell death discovery2022

DUB3/KLF4 combats tumor growth and chemoresistance in hepatocellular carcinoma.

Xuebing Jia, Lei Li, Fan Wang, Ying Xue, Tongde Wu, Qianqian Jia, Yunhui Li, Chenming Wu, Yuping Chen, Jinhuan Wu and 7 more

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

14 citing papers in PubMed, 14 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

17 authors at 6 institutions in 2 countries.

Xuebing Jia *Cancer Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China.
Lei Li *Key Laboratory of Arrhythmias of the Ministry of Education of China, Research Center for Translational Medicine, East Hospital, Tongji University School of Medicine, Shanghai, 200120, China.
Fan Wang *Cancer Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China.
Ying Xue *Zhongshan Hospital Institute of Clinical Science, Fudan University, Shanghai, 200032, China.
Tongde WuDepartment of Spine Surgery, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 200120, China.
Qianqian JiaCAS Key Laboratory of Tissue Microenvironment and Tumor, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, 200031, China.
Yunhui LiKey Laboratory of Arrhythmias of the Ministry of Education of China, Research Center for Translational Medicine, East Hospital, Tongji University School of Medicine, Shanghai, 200120, China.
Chenming WuKey Laboratory of Arrhythmias of the Ministry of Education of China, Research Center for Translational Medicine, East Hospital, Tongji University School of Medicine, Shanghai, 200120, China.
Yuping ChenKey Laboratory of Arrhythmias of the Ministry of Education of China, Research Center for Translational Medicine, East Hospital, Tongji University School of Medicine, Shanghai, 200120, China.ORCID http://orcid.org/0000-0001-8562-0804
Jinhuan WuKey Laboratory of Arrhythmias of the Ministry of Education of China, Research Center for Translational Medicine, East Hospital, Tongji University School of Medicine, Shanghai, 200120, China.
Yang SuKey Laboratory of Arrhythmias of the Ministry of Education of China, Research Center for Translational Medicine, East Hospital, Tongji University School of Medicine, Shanghai, 200120, China.
Xinshu WangBasic Medicine College, Jinzhou Medical University, Liaoning, 121000, China.
Tao ZhuangKey Laboratory of Arrhythmias of the Ministry of Education of China, Research Center for Translational Medicine, East Hospital, Tongji University School of Medicine, Shanghai, 200120, China.
Xiao DongCancer Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China.
Jing LingCancer Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China.
Jian YuanKey Laboratory of Arrhythmias of the Ministry of Education of China, Research Center for Translational Medicine, East Hospital, Tongji University School of Medicine, Shanghai, 200120, China. yuan.jian80@outlook.com.ORCID http://orcid.org/0000-0002-2801-8849
Qi LiCancer Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China. Leeqi@sjtu.edu.cn.ORCID http://orcid.org/0000-0002-2978-2339
Tongji University · CNShanghai Jiao Tong University · CNJinzhou Medical University · CNShanghai East Hospital · CNShanghai Institute of Nutrition and Health · CNSun Yat-sen University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81802754National Natural Science Foundation of China (National Science Foundation of China) 81872298National Natural Science Foundation of China (National Science Foundation of China) 91749115Natural Science Foundation of Jiangxi Province (Jiangxi Province Natural Science Foundation) 20181ACB20021Natural Science Foundation of Jiangxi Province (Jiangxi Province Natural Science Foundation) 20181BAB205044
6 · The paper itself

Abstract

This study aimed to investigate the role of deubiquitinating enzyme 3 (DUB3) in the regulation of Krüppel-like factor 4 (KLF4) expression in hepatocellular carcinoma (HCC). Gain- and loss-of-function assay, luciferase reporter assay, co-immunoprecipitation, and intracellular and extracellular deubiquitination assays were conducted in vitro. A tumor xenograft mouse model was established. The expression of DUB3 and KLF4 was examined in HCC patient specimens. The results showed that DUB3 upregulated KLF4 expression by deubiquitinating and stabilizing KLF4 protein in HCC cells through binding with KLF4. DUB3 inhibited HCC cell proliferation in vitro and tumor growth in vivo while enhancing the chemosensitivity of HCC cells in a KLF4-dependent manner. Furthermore, KLF4 promoted DUB3 transcription by binding to the DUB3 promoter. In HCC patients, DUB3 expression positively correlated with KLF4 expression in HCC tissues. Low DUB3 expression predicted worse overall survival and recurrence in HCC patients. In conclusion, this study revealed a positive DUB3/KLF4 feedback loop that inhibits tumor growth and chemoresistance in HCC. These results suggest that DUB3/KLF4 activation might be a potential therapeutic approach for HCC treatment.

Identifiers

PMID35383144
PMCPMC8983766
OpenAlexW4224308182

What OpenQuestion holds

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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.