Neuropilin and tolloid-like 2 regulates the progression of osteosarcoma
| Autor: | Wu Jiang, Xuepeng Wang, Zhenyu Bian, Liulong Zhu, Changju Hou, Maoqiang Li |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Epithelial-Mesenchymal Transition Down-Regulation Biology 03 medical and health sciences 0302 clinical medicine Downregulation and upregulation Cell Movement Cell Line Tumor Genetics Neuropilin medicine Humans Protein kinase B PI3K/AKT/mTOR pathway Cell Proliferation Osteosarcoma Oncogene Cell growth Membrane Proteins General Medicine medicine.disease Up-Regulation Gene Expression Regulation Neoplastic MicroRNAs 030104 developmental biology Cell culture 030220 oncology & carcinogenesis Disease Progression Cancer research Proto-Oncogene Proteins c-akt Signal Transduction |
| Zdroj: | Gene. 768:145292 |
| ISSN: | 0378-1119 |
| DOI: | 10.1016/j.gene.2020.145292 |
| Popis: | Neuropilin and tolloid-like 2 (NETO2) is aberrantly expressed in various malignancies. However, its role in osteosarcoma (OS) remains to be elucidated. This study aimed to identify the function of NETO2 in OS cells. The expression of NETO2 in sarcoma tissues was determined using the GEPIA database, and the mRNA and protein expression of NETO2 in OS cells and OS tissue was also assessed. The biological effects of NETO2 on OS cells were determined by overexpressing and downregulating NETO2. Cell proliferation, invasion, migration, colony formation, and epithelial-mesenchymal transition in OS cells were evaluated. Consistent with the GEPIA database, expression of NETO2 was upregulated in human OS samples and cell lines. NETO2 overexpression not only promoted the proliferation, colony formation, invasion, and epithelial-mesenchymal transition of OS cells, but also activated the PI3K/AKT signaling. NETO2 downregulation resulted in opposite effects. Furthermore, after using an AKT inhibitor, the effects of NETO2 on OS cells were attenuated. In conclusion, this study showed that NETO2 functions as an oncogene of osteosarcomas by activating the PI3K/AKT pathway. |
| Databáze: | OpenAIRE |
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