Evidence map›Paper›PMID 37039264›Full record

ArticleCancer medicine2023

Knockdown of kinesin family member 4A inhibits cell proliferation, migration, and invasion while promoting apoptosis of urothelial bladder carcinoma cells.

Chen Zhang, Maoyu Wang, Yidie Ying, Fang Meng, Hongliang Gao, Shuxiong Zeng, Yasheng Zhu, Anwei Liu, Zhensheng Zhang, Chuanliang Xu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

5 citing papers in PubMed, 4 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

10 authors at 2 institutions in 1 country.

Chen Zhang *Department of Urology, Changhai Hospital, Naval Military Medical University, Shanghai, 200433, China.
Maoyu Wang *Department of Urology, Changhai Hospital, Naval Military Medical University, Shanghai, 200433, China.
Yidie Ying *Department of Urology, Changhai Hospital, Naval Military Medical University, Shanghai, 200433, China.
Fang MengDepartment of Urology, Changhai Hospital, Naval Military Medical University, Shanghai, 200433, China.
Hongliang GaoDepartment of Urology, Changhai Hospital, Naval Military Medical University, Shanghai, 200433, China.
Shuxiong ZengDepartment of Urology, Changhai Hospital, Naval Military Medical University, Shanghai, 200433, China.
Yasheng ZhuDepartment of Urology, Changhai Hospital, Naval Military Medical University, Shanghai, 200433, China.
Anwei LiuDepartment of Critical Care Medicine, Hospital of Southern Theatre Command of PLA, Guangzhou, 510010, China.
Zhensheng ZhangDepartment of Urology, Changhai Hospital, Naval Military Medical University, Shanghai, 200433, China.ORCID 0000-0001-6578-270X
Chuanliang XuDepartment of Urology, Changhai Hospital, Naval Military Medical University, Shanghai, 200433, China.
Second Military Medical University · CNThird Affiliated Hospital of Southern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundKinesin family member 4A (KIF4A) is upregulated in a variety of cancers. However, its expression and potential downstream targets in urothelial bladder carcinoma (UBC) remain unclear.

methodsExpression data of KIF4A in UBC and noncancerous tissues were downloaded from the GEPIA database. Cell proliferation, migration, invasion, and apoptosis of T24 and 5637 UBC cells were examined using wound healing, transwell, colony formation, CCK-8, and flow cytometry assays. KIF4A and potential downstream genes were analyzed using qRT-PCR, western blot analysis, and immunohistochemistry.

resultsIn UBC samples, KIF4A expression was significantly higher than in corresponding noncancerous samples. UBC patients with high KIF4A expression had poor cancer-specific survival and overall survival. Knockdown of KIF4A significantly inhibited proliferation and promoted apoptosis of UBC cells, accompanied by dephosphorylation of AKT and increased the protein level of proapoptotic factors. Additionally, knockdown of KIF4A reduced migration and invasion of UBC cells whereas overexpression of KIF4A exhibited opposite effects, along with altered protein level in epithelial-mesenchymal transition-related genes. Furthermore, overexpression of YAP1 promoted KIF4A expression whereas knockdown of YAP1 suppressed KIF4A expression in UBC cells. Alternatively, KIF4A knockdown reduced YAP1 nuclear protein level whereas KIF4A overexpression suppressed YAP1 phosphorylation and facilitated YAP1 nuclear translocation.

conclusionsKIF4A upregulation correlates with poor prognosis of UBC. Knockdown of KIF4A inhibits proliferation, migration, and invasion of UBC cells while inducing apoptosis possibly through dephosphorylation of AKT, changes in EMT-related genes, and interaction with YAP1.

Indexed as

CarcinomaUrinary Bladder NeoplasmsApoptosisCell Line, TumorCell MovementCell ProliferationFamilyGene Expression Regulation, NeoplasticHumansKinesinsProto-Oncogene Proteins c-aktUrinary BladderKIF4A protein, humanKinesinsProto-Oncogene Proteins c-aktAKT serine/threonine kinasekinesin family member 4Aurothelial bladder carcinomaYes1 associated transcriptional regulator

Identifiers

PMID37039264
PMCPMC10278490
OpenAlexW4364353632

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.