Evidence map›Paper›PMID 28931539›Full record

ArticleAmerican journal of physiology. Cell physiology2017

Detachment-induced E-cadherin expression promotes 3D tumor spheroid formation but inhibits tumor formation and metastasis of lung cancer cells.

Phattrakorn Powan, Sudjit Luanpitpong, Xiaoqing He, Yon Rojanasakul, Pithi Chanvorachote

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  4. Review
  5. Patterned PVA Hydrogels with 3D Petri DishGels (Basel, Switzerland) · 2024
    Article
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  17. A CaMolecular cancer research : MCR · 2019
    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

5 authors at 3 institutions in 2 countries.

Phattrakorn PowanDepartment of Pharmacology and Physiology, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, Thailand.
Sudjit LuanpitpongSiriraj Center of Excellence for Stem Cell Research, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand.ORCID http://orcid.org/0000-0002-1639-4935
Xiaoqing HeDepartment of Pharmaceutical Sciences, West Virginia University, Morgantown, West Virginia; and.
Yon RojanasakulDepartment of Pharmaceutical Sciences, West Virginia University, Morgantown, West Virginia; and.
Pithi ChanvorachoteDepartment of Pharmacology and Physiology, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, Thailand; pithi_chan@yahoo.com pithi.c@chula.ac.th.
West Virginia University · USChulalongkorn University · THSiriraj Hospital · TH

Funding

Induction of Neoplastic Transformation and Cancer Stem Cells by Carbon NanotubesR01ES022968 · NIEHS · WEST VIRGINIA UNIVERSITY · PI ROJANASAKUL, YON · 2014 to 2019
$1.7M
Nanoparticle Fibrogenicity and Fibroblast Stem-Like CellsR01EB018857 · NIBIB · WEST VIRGINIA UNIVERSITY · PI ROJANASAKUL, YON · 2016 to 2019
$1.3M
NIBIB NIH HHS R01 EB018857NIEHS NIH HHS R01 ES022968
6 · The paper itself

Abstract

The epithelial-to-mesenchymal transition is proposed to be a key mechanism responsible for metastasis-related deaths. Similarly, cancer stem cells (CSCs) have been proposed to be a key driver of tumor metastasis. However, the link between the two events and their control mechanisms is unclear. We used a three-dimensional (3D) tumor spheroid assay and other CSC-indicating assays to investigate the role of E-cadherin in CSC regulation and its association to epithelial-to-mesenchymal transition in lung cancer cells. Ectopic overexpression and knockdown of E-cadherin were found to promote and retard, respectively, the formation of tumor spheroids in vitro but had opposite effects on tumor formation and metastasis in vivo in a xenograft mouse model. We explored the discrepancy between the in vitro and in vivo results and demonstrated, for the first time, that E-cadherin is required as a component of a major survival pathway under detachment conditions. Downregulation of E-cadherin increased the stemness of lung cancer cells but had an adverse effect on their survival, particularly on non-CSCs. Such downregulation also promoted anoikis resistance and invasiveness of lung cancer cells. These results suggest that anoikis assay could be used as an alternative method for in vitro assessment of CSCs that involves dysregulated adhesion proteins. Our data also suggest that agents that restore E-cadherin expression may be used as therapeutic agents for metastatic cancers.

Indexed as

AnimalsAnoikisAntigens, CDCadherinsCarcinoma, Non-Small-Cell LungCell Line, TumorEpithelial-Mesenchymal TransitionHeterograftsHumansLung NeoplasmsMiceMice, Inbred NODMice, SCIDNeoplastic Stem CellsAntigens, CDCadherinsCDH1 protein, humananoikiscancer stem cellE-cadherinepithelial-to-mesenchymal transitionlung cancermetastasistumor formation

Identifiers

PMID28931539
PMCPMC5792170
OpenAlexW2755706543

What OpenQuestion holds

Textmetadata
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.