Abstract
The bystin-like (BYSL) gene is expressed in a wide range of eukaryotes and is closely associated with tumor progression. However, its function and mechanism in osteosarcoma remain unclear. Herein, the protein expression and clinical role of BYSL in human osteosarcoma tissues were assessed. High expression of BYSL was positively related to the metastasis status and poor patient prognosis. Mechanistically, upregulation of BYSL enhanced Nrf2 expression under hypoxia in osteosarcoma cells. MicroRNAs are important epigenetic regulators of osteosarcoma development. Noteworthy, bioinformatics analysis, dual-luciferase reporter and rescue assays showed that miR-378a-3p inhibited BYSL expression by binding to its 3′-untranslated region. Analysis of miR-378a-3p function under hypoxia and normoxia showed that its upregulation suppressed osteosarcoma cells invasion and inhibited epithelial-to-mesenchymal transition by suppressing BYSL. Collectively, the results show that the miR-378a-3p/BYSL may associate with metastasis risk in osteosarcoma.
Highlights
Osteosarcoma is a common malignant bone tumor, with highly invasive and systemic metastasis, that usually occurs in children and young adults (Raymond and Jaffe, 2009; Sevelda et al, 2015)
Epithelial-to-mesenchymal transition (EMT) is characterized by a complex dynamic change, with a concomitant decline of epithelial cell markers and increased mesenchymal markers (Arias, 2001), which has been shown to contribute to cancer metastasis and invasion in osteosarcoma (Buddingh et al, 2011; Wang et al, 2017)
Since there was no clinical data on osteosarcoma in The Cancer Genome Atlas (TCGA), the sarcoma dataset was miR-378a-3p Regulates Osteosarcoma Progression selected
Summary
Osteosarcoma is a common malignant bone tumor, with highly invasive and systemic metastasis, that usually occurs in children and young adults (Raymond and Jaffe, 2009; Sevelda et al, 2015). In-depth investigations on the molecular mechanisms underlying osteosarcoma metastasis are meaningful for the research of novel treatment approaches. Epithelial-to-mesenchymal transition (EMT) promotes the transformation of early tumors into aggressive malignant tumors, especially during tumor metastasis and invasion, which is an important event in the malignant transformation of cancer cells. EMT is characterized by a complex dynamic change, with a concomitant decline of epithelial cell markers (including β-catenin and E-cadherin) and increased mesenchymal markers (including vimentin and N-cadherin) (Arias, 2001), which has been shown to contribute to cancer metastasis and invasion in osteosarcoma (Buddingh et al, 2011; Wang et al, 2017). Inhibition of EMT is a suitable therapeutic strategy for preventing osteosarcoma metastasis
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