Abstract |
Osteosarcoma (OS) is a malignant bone tumor characterized by poor prognosis due to its regional invasion and early metastasis. In this study, we aimed to find the role and the underlying mechanism of Cathepsin E (CTSE) in OS growth and metastasis. We found CTSE is upregulated in metastatic OS, rather than in the primary lesion, as confirmed by RT-qPCR and western blot analysis of clinical OS samples. Furthermore, both in vitro and in vivo experiments illustrated that CTSE promoted both growth and metastasis of OS cells, partially mediated through the modulation of Epithelial-Mesenchymal Transition (EMT). Bioinformatics analysis predicted that miR-185-5p downregulates CTSE via directly binding to the 3'UTR of CTSE, which was verified by luciferase reporter assay and rescue assays. This study reported for the first time that CTSE is a potential biomarker in OS tumorigenesis and metastasis, providing a promising therapeutic target for OS treatment.
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Authors | Yue Wu, Weili Zhou, Zhijun Yang, Jinping Li, Yi Jin |
Journal | International journal of toxicology
(Int J Toxicol)
2022 Mar-Apr
Vol. 41
Issue 2
Pg. 115-125
ISSN: 1092-874X [Electronic] United States |
PMID | 35213250
(Publication Type: Journal Article)
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Chemical References |
- MIRN185 microRNA, human
- MicroRNAs
- Cathepsin E
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Topics |
- Bone Neoplasms
(genetics, metabolism, pathology)
- Cathepsin E
(metabolism)
- Cell Line, Tumor
- Cell Movement
- Cell Proliferation
- Epithelial-Mesenchymal Transition
- Gene Expression Regulation, Neoplastic
- Humans
- MicroRNAs
(genetics, metabolism)
- Neoplasm Metastasis
- Osteosarcoma
(genetics, metabolism, pathology)
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