Evidence map›Paper›PMID 23272116›Full record

ArticlePloS one2012

Epithelial mesenchymal transition is required for acquisition of anoikis resistance and metastatic potential in adenoid cystic carcinoma.

Jun Jia, Wei Zhang, Jian-Ying Liu, Gang Chen, Hui Liu, Hao-Yan Zhong, Bing Liu, Yu Cai, Jia-Li Zhang, Yi-Fang Zhao

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
5.9field-weighted citation impact, top 4% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Immunophenotypical alterations with impact on the epithelial-mesenchymal transition (EMT) process in salivary gland adenoid cystic carcinomas.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie · 2020
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  20. Protein Kinase C-ε Promotes EMT in Breast Cancer.Breast cancer : basic and clinical research · 2014
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Jun JiaThe State Key Laboratory Breeding Base of Basic Science of Stomatology and Key Laboratory of Oral Biomedicine Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan, China.
Wei Zhang
Jian-Ying Liu
Gang Chen
Hui Liu
Hao-Yan Zhong
Bing Liu
Yu Cai
Jia-Li Zhang
Yi-Fang Zhao
Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human adenoid cystic carcinoma (ACC) is characterized by diffused invasion of the tumor into adjacent organs and early distant metastasis. Anoikis resistance and epithelial mesenchymal transition (EMT) are considered prerequisites for cancer cells to metastasize. Exploring the relationship between these processes and their underlying mechanism of action is a promising way to better understand ACC tumors. We initially established anoikis-resistant sublines of ACC cells; the variant cells revealed a mesenchymal phenotype through Slug-mediated EMT-like transformation and displayed enhanced metastatic potential both in vitro and in vivo. Suppression of EMT by knockdown of Slug significantly impaired anoikis resistance, migration, and invasion of the variant cells. With overexpression of Slug and Twist, we determined that induction of EMT in normal ACC cells could prevent anoikis, albeit partially. These findings strongly suggest that EMT is indispensable in anoikis resistance, at least in ACC cells. Furthermore, we found that the EGFR/PI3K/Akt pathway acts as the common regulator for EMT-like transformation and anoikis resistance, as confirmed by their specific inhibitors. Gefitinib and LY294003 restored the sensibilities of anoikis-resistant cells to anoikis and simultaneously impaired their metastatic potential. In addition, the results from our in vivo model of metastasis suggest that pretreatment with gefitinib promotes mouse survival by alleviating pulmonary metastasis. Most importantly, immunohistochemistry of human ACC specimens showed a correlation between the overexpression of Slug and EGFR staining. This study has demonstrated that Slug-mediated EMT-like transformation is required by human ACC cells to achieve anoikis resistance and their metastatic potential. Targeting the EGFR/PI3K/Akt pathway holds potential as a preventive strategy against distant metastasis of ACC.

Indexed as

AnoikisEpithelial-Mesenchymal TransitionAnimalsAntineoplastic AgentsApoptosisCarcinoma, Adenoid CysticCell Line, TumorCell MovementErbB ReceptorsFemaleGefitinibGene Expression Regulation, NeoplasticHumansLung NeoplasmsMiceMice, Inbred BALB CAntineoplastic AgentsErbB ReceptorsGefitinibPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktQuinazolinesSNAI1 protein, humanSnai2 protein, mouseSnail Family Transcription FactorsTranscription Factors

Identifiers

PMID23272116
PMCPMC3522696
OpenAlexW2038681263

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.