ArticleScientific reports2023
KIF2C accelerates the development of non-small cell lung cancer and is suppressed by miR-186-3p via the AKT-GSK3β-β-catenin pathway.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- KIF2C/MCAK a prognostic biomarker and its oncogenic potential in malignant progression, and prognosis of cancer patients: a systematic review and meta-analysis as biomarker.Critical reviews in clinical laboratory sciences · 2024Pooled it
- CircTMCC1 enhances radioresistance in esophageal squamous cell carcinoma by upregulating MYC via miR-186-3p sponging.Discover oncology · 2026Article
- MicroRNA-regulated signaling and tumor microenvironment modulation in lung cancer: mechanistic insights and translational opportunities.Cancer cell international · 2026Review
- Harnessing GSK-3β inhibition for lung cancer therapy: emerging opportunities and challenges.Medical oncology (Northwood, London, England) · 2025Review
- Overexpression of KIF2C amplifies tamoxifen resistance and lung metastasis of breast cancer through PLK1/C-Myc pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Elevated KIF2C Expression Drives Osteosarcoma Progression by Modulating the Wnt/β-Catenin Signaling Pathway and Contributing to an Immunosuppressive Tumor Microenvironment.Cancer medicine · 2025Article
- KIF2C promotes oral squamous cell carcinoma progression via PLK1 upregulation: implications for biomarker development and therapeutic targeting.Journal of molecular histology · 2025Article
- Identification of cellular senescence-associated genes for predicting the diagnosis, prognosis and immunotherapy response in lung adenocarcinoma via a 113-combination machine learning framework.Discover oncology · 2025Article
- Targeting Kinesins for Therapeutic Exploitation of Chromosomal Instability in Lung Cancer.Cancers · 2025Review
- Bioinformatics Analysis and Experimental Validation of Lactylation Related Genes in Lung Adenocarcinoma.Cancer management and research · 2025Article
- Research progress of kinesin family in neurological diseases.Frontiers in cellular neuroscience · 2025Review
- A Machine Learning-Derived Taurine Metabolism Signature Predicts Prognosis and Immune Landscape in Lung Adenocarcinoma via Integrative Single-Cell Analysis.Mediators of inflammation · 2025Article
- Integrated machine learning to predict the prognosis of lung adenocarcinoma patients based on SARS-COV-2 and lung adenocarcinoma crosstalk genes.Cancer science · 2025Article
- MicroRNA-203a inhibits breast cancer progression through the PI3K/Akt and Wnt pathways.Scientific reports · 2024Article
- Bioinformatics Analysis and Screening of Potential Target Genes Related to the Lung Cancer Prognosis.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2023Article
- KIF2C Deletion Causes Meiotic Abnormalities and Nonobstructive Azoospermia in Mice.Reproductive medicine and biologyArticle
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to explore how kinesin family member 2C (KIF2C) influences the progression of non-small cell lung cancer (NSCLC). The levels of KIF2C and microRNA-186-3p (miR-186-3p) were examined by quantitative real-time polymerase chain reaction (qRT-PCR). Through the utilization of cell counting kit-8 (CCK-8) assay, colony formation assay, wound closure assay, and Transwell assay, NSCLC cell proliferation, migration, and invasion were identified, respectively. NSCLC cell apoptosis was assessed using the TUNEL assay and flow cytometry (FCM) assay. Luciferase reporter analysis was used to investigate the relationship between KIF2C and miR-186-3p. Western blot assays were conducted to investigate the influence of KIF2C on the AKT-GSK3β-β-catenin pathway. The results showed that KIF2C was up-regulated in NSCLC cells, which predicted poor prognosis. KIF2C overexpression promoted the proliferation, migration, and invasion of NSCLC cells as well as inhibited NSCLC cell apoptosis. KIF2C was as a key target of miR-186-3p. High expression of KIF2C, meanwhile, increased the levels of β-catenin, p-GSK-3β and phosphorylated protein kinase B (p-AKT). KIF2C downregulation and miR-186-3p upregulation reversed these outcomes. As an oncogenic factor, KIF2C is negatively regulated by miR-186-3p and participates in the progression of NSCLC through the AKT-GSK3β-β-catenin pathway.
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