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Archive > Volume 32 Issue 8 > 2025,32(8):854-861. DOI:10.3872/j.issn.1007-385X.2025.08.009 Prev Next
Clinical Research
Versican promotes the malignant biological behaviors of lung adenocarcinoma cells via matrix metalloproteinase-9
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Abstract:
[Abstract] Objective: To investigate the roles and regulatory mechanisms of versican (VCAN) and matrix metalloproteinase-9 (MMP9) in the invasion and metastasis of lung adenocarcinoma (LUAD). Methods: Thirty LUAD specimens and their matched adjacent non-tumor tissues were collected. Immunohistochemistry (IHC) was performed to detect VCAN and MMP9 expressions. Human LUAD cell lines NCI-H1975 and A549 were employed as models. siRNA interference and plasmid overexpression, combined with rescue assays, were applied. Cell proliferation, migration, and invasion abilities were evaluated by CCK-8, scratch-healing assay, and Transwell assay, respectively. Gene and protein expression were detected by RT-qPCR and WB assay. Results: VCAN and MMP9 were significantly up-regulated in LUAD tissues compared with those in adjacent non-tumor tissues (both P < 0.001), and their H-score increased progressively with advancing tumor stage (both P < 0.01). In vitro experiments revealed that si-VCAN markedly reduced VCAN and MMP9 mRNA and protein levels and suppressed cell viability, migration, and invasion (all P < 0.01), whereas MMP9 overexpression significantly promoted these malignant phenotypes (all P < 0.001); these effects were reversed by si-VCAN (all P < 0.01). MMP9 knockdown did not significantly affect VCAN protein levels (P > 0.05). Conclusion: VCAN enhances the proliferation, migration, and invasion of LUAD cells by up-regulating MMP9. The VCAN/MMP9 axis may represent a potential therapeutic target for LUAD.
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