Evidence map›Paper›PMID 33150178›Full record

ArticleBioMed research international2020

KIF3C Promotes Proliferation, Migration, and Invasion of Glioma Cells by Activating the PI3K/AKT Pathway and Inducing EMT.

Yang Gao, Hui Zheng, Liangdong Li, Changshuai Zhou, Xin Chen, Xiaoyan Zhou, Yiqun Cao

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

15 citing papers in PubMed, 30 citations in OpenAlex.

  1. The kinesin KIF3AC recycles endocytosed integrin to polarize new adhesion formation toward the leading edge.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  2. Research progress of kinesin family in neurological diseases.Frontiers in cellular neuroscience · 2025
    Review
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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

7 authors at 2 institutions in 1 country.

Yang Gao *Department of Neurosurgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China.
Hui Zheng *Department of Nuclear Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai 200072, China.
Liangdong Li *Department of Neurosurgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China.
Changshuai ZhouDepartment of Neurosurgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China.
Xin ChenDepartment of Neurosurgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China.
Xiaoyan ZhouDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China.ORCID https://orcid.org/0000-0003-4437-0049
Yiqun CaoDepartment of Neurosurgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China.ORCID https://orcid.org/0000-0002-2997-9051
Shanghai Medical College of Fudan University · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kinesin superfamily protein 3C (KIF3C), a motor protein of the kinesin superfamily, is expressed in the central nervous system (CNS). Recently, several studies have suggested that KIF3C may act as a potential therapeutic target in solid tumors. However, the exact function and possible mechanism of the motor protein KIF3C in glioma remain unclear. In this study, a variety of tests including CCK-8, migration, invasion, and flow cytometry assays, and western blot were conducted to explore the role of KIF3C in glioma cell lines (U87 and U251). We found that overexpression of KIF3C in glioma cell lines promoted cell proliferation, migration, and invasion and suppressed apoptosis, while silencing of KIF3C reversed these effects. Ectopic KIF3C also increased the expression of N-cadherin, vimentin, snail, and slug to promote the epithelial-mesenchymal transition (EMT). Mechanistically, overexpression of KIF3C increased the levels of phosphatidylinositol 3-kinase (PI3K) and phosphorylated protein kinase B (p-AKT). These responses were reversed by KIF3C downregulation or AKT inhibition. Our results indicate that KIF3C promotes proliferation, migration, and invasion and inhibits apoptosis in glioma cells, possibly by activating the PI3K/AKT pathway

Indexed as

Gene Expression Regulation, NeoplasticAntibodies, NeutralizingAntigens, CDApoptosisCadherinsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionHumansKinesinsNeurogliaPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Small InterferingSignal TransductionAntibodies, NeutralizingAntigens, CDCadherinsCDH2 protein, humanKIF3C protein, humanKinesinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Small InterferingSNAI1 protein, humanSnail Family Transcription FactorsVimentinVIM protein, human

Identifiers

PMID33150178
PMCPMC7603552
OpenAlexW3093586638

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.