Evidence map›Paper›PMID 31378124›Full record

ArticleCell cycle (Georgetown, Tex.)2019

Silencing of EPCAM suppresses hepatic fibrosis and hepatic stellate cell proliferation in mice with alcoholic hepatitis via the PI3K/Akt/mTOR signaling pathway.

Zhi Zhang, Huiqing Wen, Jun Weng, Lei Feng, Hongya Liu, Xiaojun Hu, Fanhong Zeng

RetractedOpen access · bronzeAbstract readRetracted Publication
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 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 It has been retracted, and should not be counted.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
2.9field-weighted citation impact, top 9% 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, 26 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Zhi ZhangDepartment of Hepatobiliary Surgery, The Fifth Affiliated Hospital, Southern Medical University , Guangzhou , P. R. China.
Huiqing WenDepartment of Hepatobiliary Surgery, The Fifth Affiliated Hospital, Southern Medical University , Guangzhou , P. R. China.
Jun WengDepartment of Hepatobiliary Surgery II, Zhujiang Hospital, Southern Medical University , Guangzhou , P. R. China.
Lei FengDepartment of Hepatobiliary Surgery II, Zhujiang Hospital, Southern Medical University , Guangzhou , P. R. China.
Hongya LiuDepartment of Hepatobiliary Surgery, The Fifth Affiliated Hospital, Southern Medical University , Guangzhou , P. R. China.
Xiaojun HuDepartment of Hepatobiliary Surgery, The Fifth Affiliated Hospital, Southern Medical University , Guangzhou , P. R. China.
Fanhong ZengDepartment of Hepatobiliary Surgery II, Zhujiang Hospital, Southern Medical University , Guangzhou , P. R. China.
Third Affiliated Hospital of Southern Medical University · CNZhujiang Hospital · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alcoholic hepatitis (AH) is a severe condition developed in patients with underlying alcoholic liver disease. Epithelial cell adhesion molecule (EPCAM) plays a role in hepatitis. Therefore, the current study aimed to explore the effect of EPCAM and its potential mechanism in AH. Bioinformatic analysis was performed to screen differentially expressed genes associated with AH. AH mouse models were established through a Lieber-DeCarli liquid diet containing 4% ethanol, which were co-treated with siRNA against EPCAM or the PI3K/Akt/mTOR signaling pathway inhibitor in order to investigate the effects of EPCAM and the PI3K/Akt/mTOR signaling pathway on hepatic fibrosis, hepatic stellate cell (HSC) proliferation and apoptosis. The relationship between EPCAM and the PI3K/Akt/mTOR signaling pathway was investigated for the purposes of elucidating the potential mechanism of EPCAM in AH. EPCAM was predicted to regulate AH progression through the PI3K/Akt/mTOR signaling pathway. Silencing EPCAM or inhibition of the PI3K/Akt/mTOR signaling pathway inhibited the hepatic fibrosis and HSC proliferation yet induced HSC apoptosis. Moreover, silencing EPCAM was found to repress the PI3K/Akt/mTOR signaling pathway as evidenced by decreased levels of Bcl2 yet increased levels of caspase-3. Collectively, silencing EPCAM could hinder AH progression by inhibiting the PI3K/Akt/mTOR signaling pathway, which might serve as a potential therapeutic target for AH treatment.

Indexed as

Gene SilencingAnimalsApoptosisCell LineCell ProliferationDisease Models, AnimalEpithelial Cell Adhesion MoleculeHepatic Stellate CellsHepatitis, AlcoholicLiver Cirrhosis, AlcoholicMaleMiceMice, Inbred C57BLPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Small InterferingEpithelial Cell Adhesion MoleculemTOR protein, mousePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Small InterferingTOR Serine-Threonine Kinasesalcoholic hepatitisEpithelial cell adhesion moleculehepatic fibrosishepatic stellate cellPI3K/Akt/mTOR signaling pathwayproliferation and apoptosis

Identifiers

PMID31378124
PMCPMC6738525
OpenAlexW2965309027

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.