Evidence map›Paper›PMID 29305578›Full record

ArticleCell death & disease2018

Epithelial cell adhesion molecule overexpression regulates epithelial-mesenchymal transition, stemness and metastasis of nasopharyngeal carcinoma cells via the PTEN/AKT/mTOR pathway.

Meng-He Wang, Rui Sun, Xiao-Min Zhou, Mei-Yin Zhang, Jia-Bin Lu, Yang Yang, Li-Si Zeng, Xian-Zi Yang, Lu Shi, Ruo-Wen Xiao and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
6.7field-weighted citation impact, top 2% 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

79 citing papers in PubMed, 157 citations in OpenAlex.

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19 more citing papers are in PubMed but not listed here.

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

12 authors at 5 institutions in 1 country.

Meng-He WangState Key Laboratory of Oncology in South China, Guangzhou, China.
Rui SunDepartment of Nasopharyngeal Carcinoma, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Xiao-Min ZhouZhoukou Hospital of Traditional Chinese Medicine, Zhoukou, China.
Mei-Yin ZhangState Key Laboratory of Oncology in South China, Guangzhou, China.
Jia-Bin LuDepartment of Pathology, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Yang YangState Key Laboratory of Oncology in South China, Guangzhou, China.
Li-Si ZengCancer Center of Guangzhou Medical University, Guangzhou, China.
Xian-Zi YangCancer Center of Guangzhou Medical University, Guangzhou, China.
Lu ShiState Key Laboratory of Oncology in South China, Guangzhou, China.
Ruo-Wen XiaoState Key Laboratory of Oncology in South China, Guangzhou, China.
Hui-Yun WangState Key Laboratory of Oncology in South China, Guangzhou, China. wanghy@mail.sysu.edu.cn.
Shi-Juan MaiState Key Laboratory of Oncology in South China, Guangzhou, China. maishj@sysucc.org.cn.
Sun Yat-sen University Cancer Center · CNSun Yat-sen University · CNGuangzhou Medical University · CNState Key Laboratory of Oncology in South ChinaZhoukou City Academy of Agricultural Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial cell adhesion molecule (EpCAM) is known to be highly expressed in a variety of epithelial carcinomas, and it is involved in cell adhesion and proliferation. However, its expression profile and biological function in nasopharyngeal carcinoma (NPC) remains unclear. In this study, higher expression of EpCAM was found in NPC samples compared with non-cancer nasopharyngeal mucosa by qRT-PCR. Additionally, immunohistochemistry (IHC) analysis of NPC specimens from 64 cases showed that high EpCAM expression was associated with metastasis and shorter survival. Multivariate survival analysis identified high EpCAM expression as an independent prognostic factor. Ectopic EpCAM expression in NPC cells promoted epithelial-mesenchymal transition (EMT), induced a cancer stem cell (CSC)-like phenotype, and enhanced metastasis in vitro and in vivo without an effect on cell proliferation. Notably, EpCAM overexpression reduced PTEN expression and increased the level of AKT, mTOR, p70S6K and 4EBP1 phosphorylation. Correspondingly, an AKT inhibitor and rapamycin blocked the effect of EpCAM on NPC cell invasion and stem-like phenotypes, and siRNA targeting PTEN rescued the oncogenic activities in EpCAM knockdown NPC cells. Our data demonstrate that EpCAM regulates EMT, stemness and metastasis of NPC cells via the PTEN/AKT/mTOR pathway.

Indexed as

Adaptor Proteins, Signal TransducingAdultAnimalsCadherinsCell Cycle ProteinsCell Line, TumorCell MovementEpithelial Cell Adhesion MoleculeEpithelial-Mesenchymal TransitionFemaleHumansKaplan-Meier EstimateMaleMiceMice, NudeMiddle AgedAdaptor Proteins, Signal TransducingCadherinsCell Cycle ProteinsEIF4EBP1 protein, humanEpithelial Cell Adhesion MoleculeMTOR protein, humanPhosphoproteinsProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanRNA, Small InterferingSirolimusTOR Serine-Threonine Kinases

Identifiers

PMID29305578
PMCPMC5849035
OpenAlexW2781637114

What OpenQuestion holds

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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.