Evidence map›Paper›PMID 34723730›Full record

ArticleRenal failure2021

Implications of cell division cycle associated 4 on the Wilm's tumor cells viability via AKT/mTOR signaling pathway.

Suqing Li, Cong Qin, Yike Chen, Dan Wei, Zhijun Tan, Jiadong Meng

Open access · goldAbstract read
In one paragraph

Article in Renal failure, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 43% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. CDCA4 promotes bladder cancer progression by JAK/STAT signaling pathway.Journal of cancer research and clinical oncology · 2025
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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 3 institutions in 1 country.

Suqing LiDepartment of Pediatrics, Guigang City People's Hospital, the Eight Affiliated Hospital of Guangxi Medical University, Guigang, P.R. China.
Cong QinDepartment of Pediatrics, Guigang City People's Hospital, the Eight Affiliated Hospital of Guangxi Medical University, Guigang, P.R. China.
Yike ChenDepartment of Pediatrics, Guigang City People's Hospital, the Eight Affiliated Hospital of Guangxi Medical University, Guigang, P.R. China.
Dan WeiDepartment of Pediatrics, the First Affiliated Hospital of Guangxi Medical University, Nanning, P.R. China.
Zhijun TanDepartment of Pediatrics, Guigang City People's Hospital, the Eight Affiliated Hospital of Guangxi Medical University, Guigang, P.R. China.
Jiadong MengDepartment of Pediatrics, Guigang City People's Hospital, the Eight Affiliated Hospital of Guangxi Medical University, Guigang, P.R. China.
Guangxi Medical University · CNGuigang City People's Hospital · CNFirst Affiliated Hospital of GuangXi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe aim of present report was to elucidate the effect of cell division cycle associated 4 (CDCA4) on the proliferation and apoptosis of Wilm's tumor cells, and to further evaluate its underlying mechanism.

methodsThe expression profiles of CDCA4 and clinical information of Wilm's tumor patients were obtained from public Therapeutically Applicable Research to Generate Effective Treatments (TARGET) database portal. Real-time qPCR and western blot analyses were utilized to determine the expression levels of CDCA4. Gain- and loss-of-function of CDCA4 assays were conducted with transfection technology to investigate the biological role of CDCA4 in Wilm's tumor cells. Cell counting kit 8 and flow cytometer assays were employed to examine the effect of CDCA4 on the cells proliferation and apoptosis. Protein expression levels of indicated markers in each group of Wilm's tumor cells were measured by western blot.

resultsThe transcriptional expression of CDCA4 was drastically upregulated in Wilm's tumor tissues according to the public TARGET database and in Wilm's tumor cells. The cells viability was remarkably reduced whereas the cells apoptosis was increased in CDCA4-knockdown group compared with negative control group. However, CDCA4-overexpression group promoted the cells proliferation and suppressed the cells apoptosis. Furthermore, the protein expression levels of p-AKT, p-mTOR, and Cyclin D1 were significantly reduced after depletion of CDCA4, whereas overexpression of CDCA4 dramatically elevated these markers' expression levels.

conclusionsCDCA4 is highly expressed in Wilm's tumor and promoted the proliferation whereas inhibited the apoptosis of Wilm's tumor cells through activating the AKT/mTOR signaling pathway.

Indexed as

ApoptosisCell Cycle ProteinsCell Line, TumorCell ProliferationCell SurvivalCyclin D1HumansKidney NeoplasmsProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesWilms TumorCDCA4 protein, humanCell Cycle ProteinsCyclin D1Proto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesapoptosisCDCA4Nephroblastomaproliferation

Identifiers

PMID34723730
PMCPMC8567894
OpenAlexW3210189611

What OpenQuestion holds

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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.