Evidence map›Paper›PMID 30050313›Full record

ArticleOncoTargets and therapy2018

CEP55 promotes the proliferation, migration and invasion of esophageal squamous cell carcinoma via the PI3K/Akt pathway.

Yang Jia, Zhaohua Xiao, Xin Gongsun, Zhongwei Xin, Bin Shang, Gang Chen, Zhou Wang, Wenpeng Jiang

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

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  18. Mitotic slippage: an old tale with a new twist.Cell cycle (Georgetown, Tex.) · 2019
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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

8 authors at 1 institution in 1 country.

Yang JiaDepartment of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China, jwp1983@126.com.
Zhaohua XiaoDepartment of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China, jwp1983@126.com.
Xin GongsunDepartment of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China, jwp1983@126.com.
Zhongwei XinDepartment of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China, jwp1983@126.com.
Bin ShangDepartment of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China, jwp1983@126.com.
Gang ChenDepartment of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China, jwp1983@126.com.
Zhou WangDepartment of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China, jwp1983@126.com.
Wenpeng JiangDepartment of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China, jwp1983@126.com.
Shandong Provincial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCentrosomal protein 55 (CEP55) is an important prognostic biomarker that plays an essential role in the proliferation, migration and invasion of multiple tumors. We aimed to investigate the prognostic value of CEP55 in pN0 esophageal squamous cell carcinoma (ESCC) and explore its biological function in ESCC cells.

methodsWe used immunohistochemistry and Western blot analysis to detect the expression of CEP55 in ESCC. Furthermore, both in vitro and in vivo assays were used to determine the effect of CEP55 on malignant behavior in ESCC cells.

resultsAs expected, we found that CEP55 was overexpressed in ESCC. Univariate and multivariate analyses demonstrated that patients with CEP55 overexpression had a poor prognosis. Additionally, the abilities of proliferation, migration and invasion of cells, as well as the epithelial-mesenchymal transition markers, were all altered with the changed CEP55 expression levels in ESCC cells. Further study elucidated that CEP55 facilitated ESCC via the PI3K/Akt pathway. Blockade of this pathway markedly attenuated CEP55-mediated proliferation, migration, invasion and epithelial-mesenchymal transition of ESCC cells.

conclusionOncogenic CEP55 correlates with a poor prognosis by regulating tumor cell proliferation, migration and invasion via the PI3K/Akt pathway. It can serve as a promising prognostic biomarker and therapeutic target of pN0 ESCC after Ivor-Lewis esophagectomy.

Indexed as

CEP55esophageal squamous cell carcinomainvasionmigrationPI3K/Akt pathwayproliferation

Identifiers

PMID30050313
PMCPMC6055835
OpenAlexW2884994258

What OpenQuestion holds

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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.