Evidence map›Paper›PMID 33806040›Full record

ArticleCancers2021

Honokiol Prevents Non-Alcoholic Steatohepatitis-Induced Liver Cancer via EGFR Degradation through the Glucocorticoid Receptor-MIG6 Axis.

Keiichiro Okuda, Atsushi Umemura, Shiori Umemura, Seita Kataoka, Hiroyoshi Taketani, Yuya Seko, Taichiro Nishikawa, Kanji Yamaguchi, Michihisa Moriguchi, Yoshihiro Kanbara and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

10 citing papers in PubMed, 21 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

15 authors at 4 institutions in 2 countries.

Keiichiro OkudaDepartment of Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kamigyo-ku, Kyoto 602-8566, Japan.
Atsushi UmemuraDepartment of Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kamigyo-ku, Kyoto 602-8566, Japan.
Shiori UmemuraDepartment of Obstetrics and Gynecology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kamigyo-ku, Kyoto 602-8566, Japan.
Seita KataokaDepartment of Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kamigyo-ku, Kyoto 602-8566, Japan.
Hiroyoshi TaketaniDepartment of Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kamigyo-ku, Kyoto 602-8566, Japan.ORCID 0000-0003-1033-2642
Yuya SekoDepartment of Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kamigyo-ku, Kyoto 602-8566, Japan.ORCID 0000-0002-3658-5894
Taichiro NishikawaDepartment of Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kamigyo-ku, Kyoto 602-8566, Japan.
Kanji YamaguchiDepartment of Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kamigyo-ku, Kyoto 602-8566, Japan.ORCID 0000-0002-0631-046X
Michihisa MoriguchiDepartment of Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kamigyo-ku, Kyoto 602-8566, Japan.
Yoshihiro KanbaraDepartment of Gastroenterology and Hepatology, Saiseikai Suita Hospital, Suita 564-0013, Japan.
Jack L ArbiserDepartment of Dermatology, Emory University School of Medicine, Atlanta, GA 30322, USA.
Toshihide ShimaDepartment of Gastroenterology and Hepatology, Saiseikai Suita Hospital, Suita 564-0013, Japan.
Takeshi OkanoueDepartment of Gastroenterology and Hepatology, Saiseikai Suita Hospital, Suita 564-0013, Japan.ORCID 0000-0002-2390-3400
Michael KarinLaboratory of Gene Regulation and Signal Transduction, Departments of Pharmacology, School of Medicine, University of California San Diego, 9500 Gilman Drive, La Jolla, San Diego, CA 92093, USA.
Yoshito ItohDepartment of Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kamigyo-ku, Kyoto 602-8566, Japan.ORCID 0000-0001-9890-3635
Kyoto Prefectural University of Medicine · JPSaiseikai Suita Hospital · JPEmory University · USUniversity of California San Diego · US

Funding

The Southernearch Center for ALPD and CirrhosisP50AA011999 · NIAAA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HIDEKAZU TSUKAMOTO · 1999 to 2026
$45.8M
Immunosuppressive mechanisms responsible for development of non-viral liver cancer and control of its response to immune checkpoint inhibitorsU01AA027681 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI EL-KHOUEIRY, ANTHONY BOUTROS, KARIN, MICHAEL · 2018 to 2022
$3.6M
Role of p62/SQSTM1 in obesity-induced liver cancerR01CA211794 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KARIN, MICHAEL, MOSCAT, JORGE · 2017 to 2021
$3.6M
NCI NIH HHS #CA211794NCI NIH HHS R01 CA211794NIAAA NIH HHS P50 AA011999NIAAA NIH HHS U01 AA027681
6 · The paper itself

Abstract

Non-alcoholic steatohepatitis (NASH) has become a serious public health problem associated with metabolic syndrome. The mechanisms by which NASH induces hepatocellular carcinoma (HCC) remain unknown. There are no approved drugs for treating NASH or preventing NASH-induced HCC. We used a genetic mouse model in which HCC was induced via high-fat diet feeding. This mouse model strongly resembles human NASH-induced HCC. The natural product honokiol (HNK) was tested for its preventative effects against NASH progression to HCC. Then, to clarify the mechanisms underlying HCC development, human HCC cells were treated with HNK. Human clinical specimens were also analyzed to explore this study's clinical relevance. We found that epidermal growth factor receptor (EGFR) signaling was hyperactivated in the livers of mice with NASH and human HCC specimens. Inhibition of EGFR signaling by HNK drastically attenuated HCC development in the mouse model. Mechanistically, HNK accelerated the nuclear translocation of glucocorticoid receptor (GR) and promoted mitogen-inducible gene 6 (MIG6)/ERBB receptor feedback inhibitor 1 (ERRFI1) expression, leading to EGFR degradation and thereby resulting in robust tumor suppression. In human samples, EGFR-positive HCC tissues and their corresponding non-tumor tissues exhibited decreased

Indexed as

epidermal growth factor receptor (EGFR)glucocorticoid receptorhonokiolliver cancerMIG-6/ERRFI1

Identifiers

PMID33806040
PMCPMC8037653
OpenAlexW3137575789

What OpenQuestion holds

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LicenceCC BY
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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.