Evidence map›Paper›PMID 32323797›Full record

ArticleOncology reports2020

AREG mediates the epithelial‑mesenchymal transition in pancreatic cancer cells via the EGFR/ERK/NF‑κB signalling pathway.

Li Wang, Lili Wang, Hui Zhang, Junliang Lu, Zhiwen Zhang, Huanwen Wu, Zhiyong Liang

Abstract read
In one paragraph

Article in Oncology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
–field-weighted citation impact
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

56 citing papers in PubMed.

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  12. Amphiregulin in Fibrotic Diseases and Cancer.International journal of molecular sciences · 2025
    Review
  13. Article
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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

7 authors.

Li WangDepartment of Pathology, Peking Union Medical College Hospital, Research Center for Molecular Pathology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, P.R. China.
Lili WangDepartment of Pathology, Peking Union Medical College Hospital, Research Center for Molecular Pathology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, P.R. China.
Hui ZhangDepartment of Pathology, Peking Union Medical College Hospital, Research Center for Molecular Pathology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, P.R. China.
Junliang LuDepartment of Pathology, Peking Union Medical College Hospital, Research Center for Molecular Pathology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, P.R. China.
Zhiwen ZhangDepartment of Pathology, Peking Union Medical College Hospital, Research Center for Molecular Pathology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, P.R. China.
Huanwen WuDepartment of Pathology, Peking Union Medical College Hospital, Research Center for Molecular Pathology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, P.R. China.
Zhiyong LiangDepartment of Pathology, Peking Union Medical College Hospital, Research Center for Molecular Pathology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amphiregulin (AREG) is a member of the epidermal growth factor (EGF) family and is expressed in a plethora of cancers. The biological roles of AREG in the regulation of the epithelial‑mesenchymal transition (EMT) in pancreatic cancer remain unclear. To investigate the expression of epidermal growth factor receptor (EGFR) and AREG in pancreatic cancer cell lines, RT‑qPCR, western blot analysis, and ELISA were performed. RNAi and exogenous AREG treatment were used to alter AREG expression. Wound‑healing and Transwell assays were performed to evaluate cell migration and invasion abilities. Western blot analysis and immunofluorescence staining were utilized to detect the expression of EMT markers. The protein expression of potential key factors involved in EMT, as well as those of the ERK, AKT, STAT3 and NF‑κB pathways, were analysed by western blotting. The role of AREG in tumour growth in vivo was further determined using an orthotopic model of pancreatic cancer. Knockdown of AREG inhibited AsPC‑1 cell migration and invasion. AREG knockdown upregulated E‑cadherin but downregulated vimentin, Snail and Slug expression in AsPC‑1 cells. In addition, AREG stimulation increased cell migration, invasion and EMT in PANC‑1 cells, and an NF‑κB inhibitor decreased AREG‑induced cell migration, invasion and EMT in PANC‑1 cells. AREG stimulation increased the nuclear accumulation of NF‑κB through the EGFR/ERK signalling pathway to induce EMT. Tumour growth and metastasis were decreased by AREG silencing in an orthotopic model of pancreatic cancer. AREG may play a critical role in cell migration, invasion, and EMT by activating the EGFR/ERK/NF‑κB signalling pathway in pancreatic cancer cells.

Indexed as

AmphiregulinAnimalsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionErbB ReceptorsExtracellular Signal-Regulated MAP KinasesFemaleGene Expression Regulation, NeoplasticHumansMiceNeoplasm InvasivenessNeoplasm MetastasisNeoplasm TransplantationNF-kappa BAmphiregulinAREG protein, humanEGFR protein, humanErbB ReceptorsExtracellular Signal-Regulated MAP KinasesNF-kappa BAREGEMTERKNF-κBpancreatic cancer

Identifiers

PMID32323797
PMCPMC7107775

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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.