Evidence map›Paper›PMID 36396779›Full record

ArticleDigestive diseases and sciences2023

Aberrant NSG1 Expression Promotes Esophageal Squamous Cell Carcinoma Cell EMT by the Activation of ERK Signaling Pathway.

Xiaoqing Lin, Mingshu Tu, Yi Zhang, Wanzhen Zhuang, Liqing Cai, Liangming Zhang, Lili Yu, Zhenlong Zhang, Yi Huang

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Article in Digestive diseases and sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

Xiaoqing LinShengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, Fujian, China.
Mingshu TuShengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, Fujian, China.
Yi ZhangShengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, Fujian, China.
Wanzhen ZhuangShengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, Fujian, China.
Liqing CaiShengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, Fujian, China.
Liangming ZhangShengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, Fujian, China.
Lili YuShengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, Fujian, China.
Zhenlong ZhangShengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, Fujian, China.
Yi HuangShengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, Fujian, China. huangyi@fjsl.com.cn.ORCID http://orcid.org/0000-0001-7273-8301
Fujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeuron-specific gene family member 1 (NSG1) is a 21 kDa endosomal protein that is specifically expressed in neurons.

aimsThis study was to explore the expression of NSG1 and possible mechanism in Esophageal Squamous Cell Carcinoma (ESCC).

methodsThe Cancer Genome Atlas (TCGA) database was consulted to analyze the expression of NSG1 in ESCC. Immunohistochemistry (IHC) staining was used to evaluate NSG1 expression in ESCC cancerous tissues and matched paracancerous tissues. The CCK-8 assay, wound-healing assay, and transwell assay were used to detect the cell viability, migration, and invasion of ESCC cells. Western blot was used to assay epithelial-mesenchymal transition (EMT)-related proteins and ERK signaling pathway protein expression.

resultsThe results showed that the expression of NSG1 in ESCC cancerous tissues was higher than noncancerous tissues. Compared with negative control (NC) group, cell viability, migration. and invasion significantly increased, the expression of p-ERK in ERK signaling pathway was significantly upregulated, the expressions of mesenchymal marker Vimentin and EMT-related transcription factors including snail and slug were significantly upregulated, and the expression of epithelial marker E-cadherin was significantly downregulated in KYSE-150 cells with NSG1 overexpression. However, these effects were reversed by the ERK signaling pathway inhibitor U0126. On the other hand, TE-1 cells with NSG1 knockdown had the changes contrary to that in KYSE-150 cells with NSG1 overexpression.

conclusionNSG1 plays a potential carcinogenic role on the occurrence and progression of ESCC, and aberrant NSG1 expression might promote ESCC cell EMT by the activation of ERK signaling pathway.

Indexed as

Esophageal NeoplasmsEsophageal Squamous Cell CarcinomaCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessSignal TransductionCell biological behaviorEpithelial mesenchymal transitionERK signaling pathwayEsophageal squamous cell carcinomaNeuron-specific gene family member 1

Identifiers

PMID36396779
OpenAlexW4309263857

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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.