ArticleScientific reports2024
KIFC3 promotes the proliferation, migration and invasion of non-small cell lung cancer through the PI3K/AKT signaling pathway.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- LTB4R inhibits apoptosis and induces radiosensitivity by promoting the PI3K/AKT pathway in esophageal squamous cell carcinoma.Journal of thoracic disease · 2026Article
- PMM2 interacts with TRIM28 to recruit E2F4 and promote KIFC3-mediated tumor glycolysis and colorectal cancer progression.Oncogene · 2026Article
- Silencing of PIGU inhibits the progression of esophageal squamous cell carcinoma through the PI3K/AKT signaling pathway.Scientific reports · 2025Article
- Roles and therapeutic potential of the SLC family in prostate cancer-literature review.BMC urology · 2025Review
- Targeting Kinesins for Therapeutic Exploitation of Chromosomal Instability in Lung Cancer.Cancers · 2025Review
- Leveraging Kinesin Family as Key Regulators of Malignant Progression and the Immunometabolic Niche for Precision Oncology.Technology in cancer research & treatmentReview
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
KIFC3 is a member of the Kinesin superfamily proteins (KIFs). The role of KIFC3 in non-small cell lung cancer (NSCLC) is unknown. This study aimed to elucidate the function of KIFC3 in NSCLC and the underlying mechanism. Immunohistochemistry indicated that KIFC3 was highly expressed in NSCLC tissues and correlated with the degree of differentiation, tumor size, lymph node metastasis and TNM stage. MTT, colony formation and Transwell assays demonstrated that KIFC3 overexpression promoted the proliferation, migration and invasion of NSCLC cells in vitro, while KIFC3 knockdown led to the opposite results. The protein expression levels of PI3Kp85α and p-Akt were increased after KIFC3 overexpression, meanwhile the downstream protein expression levels such as cyclin D1, CDK4, CDK6, RhoA, RhoC and MMP2 were increased. This promotion effect could be inhibited by a specific inhibitor of the PI3K/Akt pathway, LY294002. Co-immunoprecipitation assays confirmed the interaction between endogenous/exogenous KIFC3 and PI3Kp85α. Tumor formation experiments in nude mice confirmed that KIFC3 overexpression promoted the proliferation, migration and invasion of NSCLC cells in vivo and performed its biological function through the PI3K/Akt signaling pathway.In conclusion, KIFC3 promotes the malignant behavior of NSCLC cells through the PI3K/Akt signaling pathway.
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