Evidence map›Paper›PMID 30426280›Full record

ArticleApoptosis : an international journal on programmed cell death2019

PPPDE1 promotes hepatocellular carcinoma development by negatively regulate p53 and apoptosis.

Xingwang Xie, Xueyan Wang, Weijia Liao, Ran Fei, Nan Wu, Xu Cong, Qian Chen, Lai Wei, Yu Wang, Hongsong Chen

Abstract read
PubMed Publisher
In one paragraph

Article in Apoptosis : an international journal on programmed cell death, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. mCell death & disease · 2026
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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 at 4 institutions in 1 country.

Xingwang XieChinese Center for Disease Control and Prevention, Beijing, 102206, China.
Xueyan WangPeking University People's Hospital, Peking University Hepatology Institute, Beijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Disease, Beijing, 100044, China.
Weijia LiaoLaboratory of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Guilin Medical University, Guilin, 541001, China.
Ran FeiPeking University People's Hospital, Peking University Hepatology Institute, Beijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Disease, Beijing, 100044, China.
Nan WuPeking University People's Hospital, Peking University Hepatology Institute, Beijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Disease, Beijing, 100044, China.
Xu CongPeking University People's Hospital, Peking University Hepatology Institute, Beijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Disease, Beijing, 100044, China.
Qian ChenLaboratory of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Guilin Medical University, Guilin, 541001, China.
Lai WeiPeking University People's Hospital, Peking University Hepatology Institute, Beijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Disease, Beijing, 100044, China.
Yu WangChinese Center for Disease Control and Prevention, Beijing, 102206, China. wangyu@chinacdc.cn.
Hongsong ChenPeking University People's Hospital, Peking University Hepatology Institute, Beijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Disease, Beijing, 100044, China. chenhongsong2999@163.com.
Peking University · CNPeking University People's Hospital · CNChinese Center For Disease Control and Prevention · CNGuilin Medical University · CN

Funding

Beijing Natural Science Foundation 7132186National Key Sci-Tech Special Project of China 2017ZX10203202National Key Sci-Tech Special Project of China 2018ZX10302207National Natural Science Foundation of China 81541151National Natural Science Foundation of China No. 81201569
6 · The paper itself

Abstract

We have previously identified that PPPDE1 is a deubiquitinase (DUB) belonging to a cysteine isopeptidase family. Here we sought to explore the biological significance of PPPDE1 in hepatocellular carcinoma and its underlying molecular mechanism. In the present study, we found that amplification and overexpression of PPPDE1 were associated with poor prognosis in hepatocellular carcinoma (HCC). We also demonstrated that knocking down of PPPDE1 could significantly block the clonal growth and tumorigenicity of human HCC cells, which revealed a critical role for PPPDE1 in HCC development. Furthermore, we proved that PPPDE1 is a key modulator of p53 protein level and its down stream apoptosis pathway. Taken together, these results suggested that PPPDE1 is a putative HCC driver gene and extensive studies should be conducted in the future to investigate the role of PPPDE1 in HCC and other tumors.

Indexed as

AnimalsApoptosisCarbon-Nitrogen LyasesCarcinoma, HepatocellularCell Line, TumorCell ProliferationCohort StudiesDown-RegulationGene Expression Regulation, NeoplasticHEK293 CellsHep G2 CellsHumansLiver NeoplasmsMaleMiceMice, Inbred BALB CCarbon-Nitrogen LyasesDESI2 protein, humanTP53 protein, humanTumor Suppressor Protein p53ApoptosisDriver geneHepatocellular carcinomap53PPPDE1

Identifiers

PMID30426280
OpenAlexW2900634094

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.