Evidence map›Paper›PMID 32546278›Full record

ArticleJournal of experimental & clinical cancer research : CR2020

3,3'-Diindolylmethane modulates aryl hydrocarbon receptor of esophageal squamous cell carcinoma to reverse epithelial-mesenchymal transition through repressing RhoA/ROCK1-mediated COX2/PGE

Peiyao Zhu, Huayun Yu, Kun Zhou, Yu Bai, Ruiqun Qi, Shuguang Zhang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

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  19. Inhibition of the interaction between Hippo/YAP and Akt signaling with ursolic acid and 3'3-diindolylmethane suppresses esophageal cancer tumorigenesis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023
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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

6 authors at 3 institutions in 1 country.

Peiyao ZhuDepartment of Thoracic Surgery, The First Hospital of China Medical University, No.155 North Nanjing Street, Shenyang, 110001, China.
Huayun YuDepartment of Gynecology and Obstetrics, Clinical Medical School, Shandong University, 44# Wenhua Xi Road, Jinan, 250012, China.
Kun ZhouDepartment of Thoracic Surgery, The First Hospital of China Medical University, No.155 North Nanjing Street, Shenyang, 110001, China.
Yu BaiDepartment of Thoracic Surgery, The First Hospital of China Medical University, No.155 North Nanjing Street, Shenyang, 110001, China.
Ruiqun QiDepartment of Dermatology, The First Hospital of China Medical University, No.155 North Nanjing Street, Shenyang, 110001, China. xiaoqiliumin@163.com.
Shuguang ZhangDepartment of Thoracic Surgery, The First Hospital of China Medical University, No.155 North Nanjing Street, Shenyang, 110001, China. shgzhang@cmu.edu.cn.
First Hospital of China Medical University · CNChina Medical University · CNShandong University · CN

Funding

National Outstanding Youth Science Fund Project of National Natural Science Foundation of China 81201890Scientific Research Fund of Liaoning Provincial Education Department 2013021002Scientific Research Fund of Liaoning Provincial Education Department LK201614
6 · The paper itself

Abstract

backgroundEsophageal squamous cell carcinoma (ESCC) is one of the most aggressive tumors in the world. Aryl hydrocarbon receptor (AHR) has been reported to promote tumor metastasis and epithelial-mesenchymal transition (EMT) is a vital process of conferring cancer cells capabilities of migration and invasion. However, the mechanism by which modulation of AHR can inhibit tumor metastasis remains unknown. Thus, we aim to investigate the underlying mechanism regarding reversing EMT process of ESCC through modulation of AHR.

methodsWe used AHR selective modulator 3,3'-diindolylmethane (DIM) to treat ESCC cell lines TE1 and KYSE150 so as to examine alterations of migration and invasion by wound healing and Transwell assay. Western blotting (WB) and qPCR were performed to detect relative genes and proteins changes regarding EMT process. Cell transfection was utilized for confirming pathways involved in DIM-induced reversal of EMT and in vivo assay was conducted for verification of the underlying mechanism. Co-IP assay was conducted for detecting protein-protein interactions.

resultsAHR was overexpressed in ESCC and modulation of AHR by DIM could inhibit migration and invasion as well as downregulate mesenchymal cell markers β-Catenin, Vimentin and Slug and upregulate epithelial cell marker Claudin-1. Meanwhile, synergically overexpression of AHR, RhoA and ROCK1 correlated with poor clinical outcomes. DIM could inhibit COX2/PGE

conclusionsIn brief, modulation of AHR by DIM can reverse EMT process and inhibit metastasis of ESCC through repressing RhoA/ROCK1-mediated COX2/PGE

Indexed as

Epithelial-Mesenchymal TransitionAnimalsAnticarcinogenic AgentsApoptosisBasic Helix-Loop-Helix ProteinsBiomarkers, TumorCell MovementCell ProliferationCyclooxygenase 2DinoprostoneEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaGene Expression Regulation, NeoplasticHumansIndolesMale3,3'-diindolylmethaneAHR protein, humanAnticarcinogenic AgentsBasic Helix-Loop-Helix ProteinsBiomarkers, TumorCyclooxygenase 2DinoprostoneIndolesPTGS2 protein, humanReceptors, Aryl HydrocarbonrhoA GTP-Binding ProteinRHOA protein, humanrho-Associated KinasesROCK1 protein, humanAHRCOX2DIMEMTESCCPGE2RhoAROCK1

Identifiers

PMID32546278
PMCPMC7298755
OpenAlexW3034319296

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.