Evidence map›Paper›PMID 31189746›Full record

ArticleBioscience reports2019

DEPDC1 promotes cell proliferation and suppresses sensitivity to chemotherapy in human hepatocellular carcinoma.

Chao Zhou, Pu Wang, Mengtian Tu, Yi Huang, Fei Xiong, Yue Wu

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Bioscience reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 23% 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, 23 citations in OpenAlex.

  1. Article
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  3. Review
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  7. Pan-cancer analysis ofAnnals of translational medicine · 2022
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  10. Biomarkers for Breast Adenocarcinoma Using In Silico Approaches.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  11. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Chao ZhouDepartment of Gastroenterology, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu 610072, China.
Pu WangDepartment of Gastroenterology, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu 610072, China.
Mengtian TuDepartment of Gastroenterology, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu 610072, China.
Yi HuangDepartment of Laboratory Medicine, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu 610072, China.
Fei XiongDepartment of Gastroenterology, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu 610072, China.
Yue WuDepartment of Pharmacy, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu 610072, China ywu0813@163.com.ORCID 0000-0003-0119-1454
Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatocellular carcinoma (HCC) is one of the major causes of tumor-related morbidity and mortality worldwide. Accumulating evidence has revealed that aberrant expression of crucial cancer-related genes contributes to hepatocellular carcinogenesis. This study aimed to characterize the biological role of DEP domain containing 1 (DEPDC1), a novel cancer-related gene, in HCC and illuminate the potential molecular mechanisms involved. MATERIALS AND

methodsQuantitative real-time PCR (qRT-PCR), Western blotting and immunohistochemical (IHC) staining were used to characterize the expression patterns of DEPDC1 in tumorous tissues and adjacent normal tissues. Kaplan-Meier survival analysis was launched to evaluate the relationship between DEPDC1 expression and overall survival. CCK8 assay, colony formation and flow cytometry were performed to investigate the effects of DEPDC1 on HCC cell viability, clonogenic capability and cell apoptosis. Murine xenograft models were established to determine the effect of DEPDC1 on tumor growth

resultsDEPDC1 was significantly up-regulated in HCC tissues compared with para-cancerous tissues. Besides, patients with high DEPDC1 expression experienced a significantly shorter overall survival. Functional investigations demonstrated that DEPDC1 overexpression facilitated HCC cell proliferation and suppressed cell apoptosis, whereas DEPDC1 depletion inhibited cell proliferation and promoted cell apoptosis. Furthermore, DEPDC1 ablation suppressed tumorigenecity of HCC cells in murine xenograft models. Mechanistic studies uncovered that JNK signaling pathway mediated the promoting effects of DEPDC1 on HCC cell viability and chemotherapy resistance.

conclusionCollectively, our data may provide some evidence for DEPDC1 as a candidate therapeutic target for HCC.

Indexed as

AgedAnimalsAnthracenesAntineoplastic AgentsApoptosisCarcinoma, HepatocellularCell ProliferationDrug Resistance, NeoplasmFemaleGene Expression Regulation, NeoplasticGTPase-Activating ProteinsHep G2 CellsHumansKaplan-Meier EstimateLiver NeoplasmsMaleAnthracenesAntineoplastic AgentsDEPDC1 protein, humanGTPase-Activating ProteinsNeoplasm Proteinspyrazolanthronecell proliferationchemotherapy resistanceDEPDC1hepatocellular carcinomaJNK signaling pathway

Identifiers

PMID31189746
PMCPMC6620382
OpenAlexW2953151118

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.