Knockdown of YKL-40 inhibits angiogenesis through regulation of VEGF/VEGFR2 and ERK1/2 signaling in endometrial cancer
| Autor: | Qin Luo, Jiang-Tao Fan, Zhao-Yu Zhou, Yan-Lu Luo, Hong-Yan Chen |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
musculoskeletal diseases
Vascular Endothelial Growth Factor A Small interfering RNA Angiogenesis MAP Kinase Signaling System Mice Nude chemistry.chemical_compound Mice Cell Movement Human Umbilical Vein Endothelial Cells Animals Humans Chitinase-3-Like Protein 1 Phosphorylation Cell Proliferation Tube formation Mice Inbred BALB C Neovascularization Pathologic Chemistry Kinase insert domain receptor Cell Biology General Medicine Transfection Vascular Endothelial Growth Factor Receptor-2 Endometrial Neoplasms Vascular endothelial growth factor Vascular endothelial growth factor A Cancer research Female Signal transduction Signal Transduction |
| Zdroj: | Cell biology internationalREFERENCES. 45(12) |
| ISSN: | 1095-8355 |
| Popis: | Studies have demonstrated that small interfering RNA (siRNA) targeting YKL-40 (siYKL-40) inhibits the proliferation, migration, invasion and induces anti-apoptotic abilities of endometrial cancer (EC) HEC-1A cells. However, its effect on angiogenesis is unclear. The present study aimed to investigate the role of YKL-40 in endometrial cancer and the related molecular mechanisms. YKL-40 was knocked down by transfection with siYKL-40 and the effects on angiogenesis, cell viability and signaling pathways were investigated. The results showed that siYKL-40 inhibited VEGFA levels and tube formation in endothelial cells. Additionally, inhibition of YKL-40 decreased the expression levels of vascular endothelial growth factor (VEGF), phosphorylated vascular endothelial growth factor receptor 2 (pVEGFR2) and phosphorylated extracellular signal-regulated kinases 1 and 2 (pERK1/2). Furthermore, a nude mice xenograft model of EC showed that siYKL-40 inhibited tumor growth. Inhibition of YKL-40 led to suppression of angiogenesis and reduction of microvessel density through VEGF/VEGFR2 and ERK1/2 signaling in endometrial cancer cells. Taken together, this study demonstrated novel molecular mechanisms for role of YKL-40 in EC. This article is protected by copyright. All rights reserved. |
| Databáze: | OpenAIRE |
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