ArticleJournal of molecular histology2025
KIF2C promotes oral squamous cell carcinoma progression via PLK1 upregulation: implications for biomarker development and therapeutic targeting.
Article in Journal of molecular histology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
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Who cites it
1 citing paper in PubMed.
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Oral squamous cell carcinoma (OSCC) is a highly aggressive malignancy with poor prognosis due to late detection, rapid progression, and frequent metastasis, underscoring the urgent need for novel therapeutic targets. This study investigates the roles of kinesin family member 2C (KIF2C) and Polo-like kinase 1 (PLK1) in OSCC progression and their functional interplay. Immunohistochemical and western blot analyses revealed marked upregulation of KIF2C and PLK1 in human OSCC tissues and cell lines (SCC9, SCC25, Cal27). Functional characterization in Cal27 cells (selected for highest KIF2C expression via qPCR/WB) demonstrated that KIF2C knockdown via siRNA transfection suppressed proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT), while inducing apoptosis and G0/G1 cell cycle arrest. Mechanistically, KIF2C silencing downregulated PLK1 expression, concomitantly reducing EMT markers (N-cadherin, vimentin), matrix metalloproteinases (MMP-2/9), and angiogenesis factors (VEGF, α-SMA). Complementary assays (CCK-8, EdU, Transwell, wound healing) and flow cytometry confirmed that KIF2C-PLK1 axis promotes tumor growth by enhancing matrix degradation, angiogenesis, and S-phase proliferation while inhibiting apoptosis. These findings establish KIF2C as a pivotal regulator of OSCC progression through PLK1-mediated signaling, highlighting their dual potential as prognostic biomarkers and therapeutic targets for OSCC management.
Indexed as
Identifiers
40293559What Socratic holds
Registered trials
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.