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ORIGINAL RESEARCH article

Front. Oncol.
Sec. Gynecological Oncology
Volume 14 - 2024 | doi: 10.3389/fonc.2024.1466264

Vitronectin promotes proliferation and metastasis of cervical cancer cells via the epithelial-mesenchymal transition

Provisionally accepted
Yao Lin Yao Lin Lihong Bian Lihong Bian Guangwei Zhu Guangwei Zhu Bin Zhang Bin Zhang *
  • gynecology and obstetrics, First Affiliated Hospital of Fujian Medical University, Fuzhou, China

The final, formatted version of the article will be published soon.

    Background: 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). Materials and methods: 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 evalue 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. Results: 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). Conclusion: VTN plays a tumor-promoting role in CC by promoting the EMT of cervical cancer cells.

    Keywords: Vitronectin, cervical cancer, proliferation, metastasis, Epithelial-mesenchymal transition EMT

    Received: 17 Jul 2024; Accepted: 15 Nov 2024.

    Copyright: © 2024 Lin, Bian, Zhu and Zhang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Bin Zhang, gynecology and obstetrics, First Affiliated Hospital of Fujian Medical University, Fuzhou, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.