Evidence map›Paper›PMID 30607788›Full record

ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2019

CEP55 promotes epithelial-mesenchymal transition in renal cell carcinoma through PI3K/AKT/mTOR pathway.

H Chen, D Zhu, Z Zheng, Y Cai, Z Chen, W Xie

Open access · hybridAbstract read
PubMed Publisher
In one paragraph

Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

33 citing papers in PubMed, 70 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

6 authors at 1 institution in 1 country.

H ChenDepartment of Urology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, 510000, China.
D ZhuDepartment of Urology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, 510000, China.
Z ZhengDepartment of Urology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, 510000, China.
Y CaiDepartment of Urology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, 510000, China.
Z ChenDepartment of Urology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, 510000, China.
W XieDepartment of Urology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, 510000, China. xiewl@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0001-5222-0767
Sun Yat-sen University · CN

Funding

Guangdong Natural Science Foundation 2014A030310133Guangdong Science and Technology Department 2013B021800110Guangdong Science and Technology Department 2015B050501004Key Laboratory of Malignant Tumor Gene Regulation and Target Therapy of Guangdong Higher Education Institutes KLB09001Key Laboratory of Malignant Tumor Molecular Mechanism and Translational Medicine of Guangzhou Bureau of Science and Information Technology [2013]163National Natural Science Foundation of China 81472388National Natural Science Foundation of China 81672534
6 · The paper itself

Abstract

purposeTo study the detailed mechanisms of tumorigenesis and clinical outcomes of centrosomal protein 55 (CEP55) overexpression in renal cell carcinoma. MATERIALS AND

methodsMicroarray analysis was performed to explore differentially expressed genes in five pairs of RCC tissues. Data of CEP55 expression and corresponding clinical information for 532 RCC patients of TCGA database were downloaded from cBioPortal. The expression of CEP55 in RCC tissues and cells was determined by real-time quantitative reverse transcription PCR (qRT-PCR), Western blot analysis and immunohistochemistry (IHC). Cells were transfected with siRNAs or lentivirus to regulate the expression of CEP55. The effects of CEP55 on proliferation, migration, invasion and epithelial-to-mesenchymal transition (EMT) of RCC cells were determined by MTS, migration and invasion assay and Western blot analysis.

resultsCEP55, one of the most upregulated genes in microarray analysis, was overexpressed in RCC tissues and cells. CEP55 expression was significantly correlated with poor outcome including neoplasm disease stage, histologic grade and TNM status, as well as survival status of patients. In vitro experiments showed that downregulation of CEP55 could dramatically inhibit RCC cell proliferation, migration and invasion, while overexpression of CEP55 could promote these biological behaviors. We further demonstrated that CEP55 knockdown suppressed epithelial-mesenchymal transition (EMT), which was mediated via upregulation of E-cadherin and downregulation of N-cadherin and ZEB1, through PI3K/AKT/mTOR pathway. In contrast, overexpression of CEP55 could promote EMT in RCC cells via the activation of PI3K/AKT/mTOR pathway. Importantly, inhibition of PI3K/AKT/mTOR pathway reduced the effects of CEP55 on the migration, invasion and EMT of RCC cells.

conclusionOur study showed that CEP55 could promote EMT through PI3K/AKT/mTOR pathway and might be an effective prognostic marker in RCC.

Indexed as

Epithelial-Mesenchymal TransitionBiomarkers, TumorCarcinoma, Renal CellCell Cycle ProteinsCell MovementCell ProliferationCell Transformation, NeoplasticFemaleFollow-Up StudiesGene Expression Regulation, NeoplasticHumansKidney NeoplasmsMaleMiddle AgedPhosphatidylinositol 3-KinasesPrognosisBiomarkers, TumorCell Cycle ProteinsCep55 protein, humanMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesCEP55Epithelial–mesenchymal transitionMetastasisProliferationRenal cell carcinoma

Identifiers

PMID30607788
OpenAlexW2907001574

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.