KIF2C promotes oral squamous cell carcinoma progression via PLK1 upregulation: implications for biomarker development and therapeutic targeting

IF 2.9 4区生物学 Q3 CELL BIOLOGY

Journal of Molecular Histology Pub Date : 2025-04-28 DOI:10.1007/s10735-025-10415-5

Chenfei Wang, Yuyuan Su, Jinlong Shi, Guijuan Feng

{"title":"KIF2C promotes oral squamous cell carcinoma progression via PLK1 upregulation: implications for biomarker development and therapeutic targeting","authors":"Chenfei Wang, Yuyuan Su, Jinlong Shi, Guijuan Feng","doi":"10.1007/s10735-025-10415-5","DOIUrl":null,"url":null,"abstract":"<div><p>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.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9000,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Molecular Histology","FirstCategoryId":"99","ListUrlMain":"https://link.springer.com/article/10.1007/s10735-025-10415-5","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}

引用次数: 0

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.

查看原文本刊更多论文

KIF2C通过PLK1上调促进口腔鳞状细胞癌的进展：对生物标志物开发和治疗靶向的影响

口腔鳞状细胞癌（Oral squamous cell carcinoma， OSCC）是一种发现晚、进展快、转移频繁、预后差的高侵袭性恶性肿瘤，迫切需要新的治疗靶点。本研究探讨了激酶家族成员2C （KIF2C）和polo样激酶1 （PLK1）在OSCC进展中的作用及其功能相互作用。免疫组织化学和western blot分析显示，KIF2C和PLK1在人OSCC组织和细胞系中显著上调（SCC9, SCC25, Cal27）。Cal27细胞（通过qPCR/WB选择KIF2C表达最高的细胞）的功能表征表明，通过转染siRNA敲低KIF2C可抑制增殖、迁移、侵袭和上皮间质转化（EMT），同时诱导细胞凋亡和G0/G1细胞周期阻滞。在机制上，KIF2C沉默会下调PLK1的表达，同时降低EMT标记物（N-cadherin, vimentin），基质金属蛋白酶（MMP-2/9）和血管生成因子（VEGF, α-SMA）。互补试验（CCK-8、EdU、Transwell、伤口愈合）和流式细胞术证实，KIF2C-PLK1轴通过增强基质降解、血管生成和s期增殖促进肿瘤生长，同时抑制细胞凋亡。这些发现表明，KIF2C通过plk1介导的信号传导，是OSCC进展的关键调节因子，突出了它们作为预后生物标志物和OSCC治疗靶点的双重潜力。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Journal of Molecular Histology 生物-细胞生物学

CiteScore

5.90

自引率

0.00%

发文量

审稿时长

1 months

期刊介绍： The Journal of Molecular Histology publishes results of original research on the localization and expression of molecules in animal cells, tissues and organs. Coverage includes studies describing novel cellular or ultrastructural distributions of molecules which provide insight into biochemical or physiological function, development, histologic structure and disease processes. Major research themes of particular interest include: - Cell-Cell and Cell-Matrix Interactions; - Connective Tissues; - Development and Disease; - Neuroscience. Please note that the Journal of Molecular Histology does not consider manuscripts dealing with the application of immunological or other probes on non-standard laboratory animal models unless the results are clearly of significant and general biological importance. The Journal of Molecular Histology publishes full-length original research papers, review articles, short communications and letters to the editors. All manuscripts are typically reviewed by two independent referees. The Journal of Molecular Histology is a continuation of The Histochemical Journal.