Evidence map›Paper›PMID 32190688›Full record

ArticleBioMed research international2020

Isoliquiritigenin Suppressed Esophageal Squamous Carcinoma Growth by Blocking EGFR Activation and Inducing Cell Cycle Arrest.

Liping Ye, Junjie Zhang, Yu Zhang, Binbin Gu, Hongyuan Zhu, Xinli Mao

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
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

6 authors at 2 institutions in 1 country.

Liping YeDepartment of Gastroenterology, Affiliated Tai Zhou Hospital of Wenzhou Medical University, No.150 Ximen Road, Linhai City, Taizhou 317000, China.
Junjie ZhangDepartment of Gastroenterology, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, China.ORCID https://orcid.org/0000-0001-8992-3271
Yu ZhangDepartment of Gastroenterology, Affiliated Tai Zhou Hospital of Wenzhou Medical University, No.150 Ximen Road, Linhai City, Taizhou 317000, China.ORCID https://orcid.org/0000-0002-5522-3178
Binbin GuDepartment of Gastroenterology, Affiliated Tai Zhou Hospital of Wenzhou Medical University, No.150 Ximen Road, Linhai City, Taizhou 317000, China.ORCID https://orcid.org/0000-0003-3005-8150
Hongyuan ZhuDepartment of Gastroenterology, Affiliated Tai Zhou Hospital of Wenzhou Medical University, No.150 Ximen Road, Linhai City, Taizhou 317000, China.ORCID https://orcid.org/0000-0001-8645-3833
Xinli MaoDepartment of Gastroenterology, Affiliated Tai Zhou Hospital of Wenzhou Medical University, No.150 Ximen Road, Linhai City, Taizhou 317000, China.ORCID https://orcid.org/0000-0001-7411-7218
Wenzhou Medical University · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Isoliquiritigenin (ILQ) is a natural product isolated from licorice root which has served as traditional Chinese medicine for a long time. Recently, the antitumor effects of ILQ have been widely studied in various cancers, but the role and related mechanisms of ILQ in esophageal squamous carcinoma cells (ESCC) are still poorly understood. In our studies, ILQ showed profound antitumor activities in ESCC cells. In vitro, ILQ substantially inhibited cell proliferation and anchorage-independent growth in a panel of human ESCC cells. Mechanism studies showed that EGFR signaling pathway played an important role for ILQ to exert its antitumor activity in ESCC. Exposure to isoliquiritigenin substantially decreased EGF-induced EGFR activation and its downstream Akt and ERK1/2 signaling pathway. EGFR knockdown with shRNA in ESCC cell significantly reduced the sensitivity of cancer cells to ILQ. Moreover, it was found that ILQ had a significantly inhibitory effect on AP-1 family, the protein of Jun and Fos subfamilies was substantially downregulated, and the transcriptional activity of AP-1 family was dramatically suppressed by ILQ. By reducing the expression of cyclin D1, ESCC cells were induced G0/G1 arrest, and cell division was substantially blocked. Finally, the antitumor potency of ILQ was validated in xenograft models and the tumor growth was prominently restrained by ILQ. Briefly, our study showed that ILQ, or its analogue, appeared to be a promising new therapeutic agent for ESCC management.

Indexed as

AnimalsAntineoplastic AgentsCell Cycle CheckpointsCell Line, TumorCell ProliferationChalconesCyclin D1Down-RegulationErbB ReceptorsEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaFemaleG1 PhaseGene Knockdown TechniquesGlycyrrhizaHumansAntineoplastic AgentsCCND1 protein, humanChalconesCyclin D1EGFR protein, humanErbB ReceptorsisoliquiritigeninProtein Kinase Inhibitors

Identifiers

PMID32190688
PMCPMC7063883
OpenAlexW3006793524

What OpenQuestion holds

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LicenceCC BY
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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.