Evidence map›Paper›PMID 38658931›Full record

ArticleCancer cell international2024

CDCA5-EEF1A1 interaction promotes progression of clear cell renal cell carcinoma by regulating mTOR signaling.

Xun Wang, An Shi, Jie Liu, Wen Kong, Yiran Huang, Wei Xue, Fan Yang, Jiwei Huang

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

3 citing papers in PubMed, 1 citations in OpenAlex.

  1. Article
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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.

Xun Wang *Department of Urology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, 200127, China.
An Shi *Department of Critical Care Medicine, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, 200127, China.
Jie Liu *Department of Pharmacy, Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Wen KongDepartment of Urology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, 200127, China.
Yiran HuangDepartment of Urology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, 200127, China.
Wei XueDepartment of Urology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, 200127, China.
Fan YangDepartment of Pharmacy, Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China. yang-fan@sjtu.edu.cn.
Jiwei HuangDepartment of Urology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, 200127, China. huangjiwei@renji.com.
Renji Hospital · CN

Funding

the National Key Research and Development Program of China 2022YFC2804300
6 · The paper itself

Abstract

backgroundCell division cycle associated 5 (CDCA5) plays ontogenetic role in various human cancers. However, its specific function and regulatory mechanism in ccRCC remain uncertain.

methodsImmunohistochemistry and western blots were performed to investigate the expression of CDCA5 in ccRCC tissues. Genetic knockdown and upregulation of CDCA5 were performed to investigate its functional roles in ccRCC proliferation, migration, apoptosis and sunitinib resistance. Furthermore, Co-IP assay and LC-MS/MS were performed to investigate the underlying mechanisms.

resultsWe found that CDCA5 expression is frequently upregulated in ccRCC tumors and is associated with poor prognosis of ccRCC patients. Functionally, CDCA5 promotes proliferation, migration, and sunitinib resistance, while inhibiting apoptosis in ccRCC cells. In vivo mouse xenograft model confirms that silencing of CDCA5 drastically inhibits the growth of ccRCC. Mechanistically, we discovered that CDCA5 interacts with Eukaryotic Translation Elongation Factor 1 Alpha 1 (EEF1A1) to regulate mTOR signaling pathway, thereby promoting ccRCC progression.

conclusionsTaken together, our results demonstrate the significant role of CDCA5 in ccRCC progression. The findings may provide insights for the development of new treatment strategies targeting CDCA5 for ccRCC patients.

Indexed as

CACD5Clear cell renal cell carcinomaEEF1A1Kidney cancermTOR

Identifiers

PMID38658931
PMCPMC11044369
OpenAlexW4395069221

What OpenQuestion holds

Textmetadata
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.