Evidence map›Paper›PMID 30794613›Full record

ArticlePloS one2019

Autophagic flux modulation by Wnt/β-catenin pathway inhibition in hepatocellular carcinoma.

Lilia Turcios, Eduardo Chacon, Catherine Garcia, Pedro Eman, Virgilius Cornea, Jieyun Jiang, Brett Spear, Chunming Liu, David S Watt, Francesc Marti and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

26 citing papers in PubMed, 47 citations in OpenAlex.

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  15. Autophagy in liver diseases.World journal of hepatology · 2021
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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

11 authors at 1 institution in 1 country.

Lilia TurciosDepartment of Surgery, Transplant Center, College of Medicine, University of Kentucky, Lexington, Kentucky, United States of America.
Eduardo ChaconDepartment of Surgery, Transplant Center, College of Medicine, University of Kentucky, Lexington, Kentucky, United States of America.
Catherine GarciaDepartment of Surgery, Transplant Center, College of Medicine, University of Kentucky, Lexington, Kentucky, United States of America.
Pedro EmanDepartment of Surgery, Transplant Center, College of Medicine, University of Kentucky, Lexington, Kentucky, United States of America.ORCID 0000-0001-6236-1723
Virgilius CorneaDepartment of Surgery, Transplant Center, College of Medicine, University of Kentucky, Lexington, Kentucky, United States of America.
Jieyun JiangLucille Parker Markey Cancer Center, University of Kentucky, Lexington, Kentucky, United States of America.
Brett SpearLucille Parker Markey Cancer Center, University of Kentucky, Lexington, Kentucky, United States of America.
Chunming LiuLucille Parker Markey Cancer Center, University of Kentucky, Lexington, Kentucky, United States of America.
David S WattLucille Parker Markey Cancer Center, University of Kentucky, Lexington, Kentucky, United States of America.
Francesc MartiDepartment of Surgery, Transplant Center, College of Medicine, University of Kentucky, Lexington, Kentucky, United States of America.
Roberto GedalyDepartment of Surgery, Transplant Center, College of Medicine, University of Kentucky, Lexington, Kentucky, United States of America.ORCID 0000-0003-4958-0918
University of Kentucky · US

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI Jennifer F Rogers · 2013 to 2026
$38.3M
NCI NIH HHS P30 CA177558
6 · The paper itself

Abstract

Autophagy targets cellular components for lysosomal-dependent degradation in which the products of degradation may be recycled for protein synthesis and utilized for energy production. Autophagy also plays a critical role in cell homeostasis and the regulation of many physiological and pathological processes and prompts this investigation of new agents to effect abnormal autophagy in hepatocellular carcinoma (HCC). 2,5-Dichloro-N-(2-methyl-4-nitrophenyl) benzenesulfonamide (FH535) is a synthetic inhibitor of the Wnt/β-catenin pathway that exhibits anti-proliferative and anti-angiogenic effects on different types of cancer cells. The combination of FH535 with sorafenib promotes a synergistic inhibition of HCC and liver cancer stem cell proliferation, mediated in part by the simultaneous disruption of mitochondrial respiration and glycolysis. We demonstrated that FH535 decreased HCC tumor progression in a mouse xenograft model. For the first time, we showed the inhibitory effect of an FH535 derivative, FH535-N, alone and in combination with sorafenib on HCC cell proliferation. Our study revealed the contributing effect of Wnt/β-catenin pathway inhibition by FH535 and its derivative (FH535-N) through disruption of the autophagic flux in HCC cells.

Indexed as

AnimalsAntineoplastic AgentsAutophagybeta CateninCarcinoma, HepatocellularCell Line, TumorCell ProliferationFemaleGene Knockdown TechniquesHumansLiver NeoplasmsLiver Neoplasms, ExperimentalMiceMice, NudeSorafenibSulfonamidesAntineoplastic Agentsbeta CateninCTNNB1 protein, humanFH535SorafenibSulfonamides

Identifiers

PMID30794613
PMCPMC6386480
OpenAlexW2915246156

What Socratic 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 Socratic graph.