Lin Yao, Bian Lihong, Zhu Guangwei, Zhang Bin
Department of Gynecology and Obstetrics, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Department of Gynecology and Obstetrics, National Regional Medical Center, Binhai Campus of the First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Front Oncol. 2024 Dec 9;14:1466264. doi: 10.3389/fonc.2024.1466264. eCollection 2024.
Vitronectin (VTN) is a multifunctional glycoprotein in blood and the extracellular, which could be an effective biomarker for many cancers. However, its role in cervical cancer is under investigated. In this study, we aimed to determine the molecular function of VTN and its potential mechanism in cervical cancer (CC).
Up- and down-regulated VTN expression was determined in Hela and C33A cells. Reverse transcription, qRT-PCR, and Western blotting test were performed to identify VTN mRNA and protein levels, separately. CCK-8 assay and colony formation assay were carried out to evaluate proliferation abilities of CC cells. A scratch test and a transwell chamber assay were performed to determine cell migration and invasion ability. Expression levels of epithelial-mesenchymal transition (EMT)-related proteins were measured by Western blotting.
Cell models with up- and down-regulated VTN expression in Hela and C33A cells were successfully established, as confirmed by Western blotting and qPCR. CCK-8 and colony formation assays demonstrated that VTN overexpression significantly enhanced the proliferation of both Hela and C33A cells. Wound healing and Transwell migration assays further indicated that VTN overexpression markedly promoted the migratory and invasive capabilities of these cells. Moreover, Western blotting analysis revealed that VTN overexpression led to a decrease in ZO-1 and E-cadherin protein levels and an increase in β-catenin and N-cadherin levels, whereas VTN knockdown yielded the opposite effect. These findings suggest that VTN promotes cervical cancer cell malignancy through epithelial-mesenchymal transition (EMT).
VTN plays a tumor-promoting role in CC by promoting the EMT of cervical cancer cells.
玻连蛋白（VTN）是血液和细胞外的一种多功能糖蛋白，可能是多种癌症的有效生物标志物。然而，其在宫颈癌中的作用尚在研究中。在本研究中，我们旨在确定VTN在宫颈癌（CC）中的分子功能及其潜在机制。
在Hela和C33A细胞中测定VTN表达的上调和下调情况。分别进行逆转录、qRT-PCR和蛋白质印迹试验以鉴定VTN的mRNA和蛋白质水平。进行CCK-8试验和集落形成试验以评估CC细胞的增殖能力。进行划痕试验和Transwell小室试验以确定细胞迁移和侵袭能力。通过蛋白质印迹法测量上皮-间质转化（EMT）相关蛋白的表达水平。
通过蛋白质印迹法和qPCR证实，成功建立了Hela和C33A细胞中VTN表达上调和下调的细胞模型。CCK-8和集落形成试验表明，VTN过表达显著增强了Hela和C33A细胞的增殖。伤口愈合和Transwell迁移试验进一步表明，VTN过表达显著促进了这些细胞的迁移和侵袭能力。此外，蛋白质印迹分析显示，VTN过表达导致ZO-1和E-钙黏蛋白水平降低，β-连环蛋白和N-钙黏蛋白水平升高，而VTN敲低则产生相反的效果。这些发现表明，VTN通过上皮-间质转化（EMT）促进宫颈癌细胞的恶性程度。
VTN通过促进宫颈癌细胞的EMT在CC中发挥促肿瘤作用。
