Long noncoding RNAs (LncRNAs) have been reported to participate in cancer development, including osteosarcoma. Here, in our study, we observed that lncRNA metastasis-associated lung adenocarcinoma transcription 1 (MALAT1) was remarkably overexpressed in osteosarcoma. However, the role it plays in osteosarcoma proliferation mediated by miR-206/cyclin-dependent kinase 9 (CDK9) axis remains uninvestigated. It was found that miR-206 was decreased and CDK9 was elevated in human osteosarcoma cells including MG63, Saos-2, U2OS, and KHOS compared with human osteoblast cell line hFOB 1.19. In addition, it was exhibited that knockdown of MALAT1 was able to inhibit osteosarcoma cell proliferation, which suggested that MALAT1 played an oncogenic role in osteosarcoma development. Bioinformatics analysis indicated that MALAT1 can function as a competing endogenous RNA by sponging miR-206. Because miR-206 has been identified as a significant tumor suppressive gene in multiple cancers, we validated that mimics of miR-206 can restrain osteosarcoma progression. Furthermore, dual-luciferase reporter assay, RNA binding protein immunoprecipitation, and RNA pull-down assay demonstrated the correlation between miR-206 and MALAT1. Besides these, CDK9 was predicted as a downstream gene of miR-206, and we observed that MALAT1 can regulate osteosarcoma progress by modulating CDK9 expression via sponging miR-206. In conclusion, our study implied that MALAT1/miR-206/CDK9 axis can provide novel insights into the biological mechanism of osteosarcoma progression.
Background: Platelets are associated with poor prognosis in most tumors, but their specific pathogenic mechanism in osteosarcoma is not yet clear. The objective of this study is to conduct an in-depth analysis of how genes closely related to platelet function impact the prognosis of osteosarcoma patients. We hope that through this research, we can uncover the potential mechanisms of these genes in the development and progression of osteosarcoma, thereby providing new therapeutic strategies and theoretical foundations for improving the prognosis of osteosarcoma patients.
Osteosarcoma (OS) is the most common primary malignant bone tumor in childhood. Patients who present with metastatic disease at diagnosis or relapse have a very poor prognosis, and this has not changed over the past four decades. The Wnt signaling pathway plays a role in regulating osteogenesis and is implicated in OS pathogenesis.
Osteosarcoma (OS) is a rare form of malignant bone tumor affecting jaws. The diagnosis of jaws osteosarcoma (JO) presents a unique challenge due to its rarity and the diversity of histological presentations it can exhibit. Fibroblastic osteosarcoma (FO), a subtype of OS, is characterized by the presence of fibroblastic cells and osteoid-producing cells within the tumor matrix.
Background: Osteosarcoma is a malignant tumor originating from mesenchymal bone tissue, characterized by high malignancy and poor prognosis. Despite progress in comprehensive treatment approaches, the five-year survival rate remains largely unchanged, highlighting the need to clarify its underlying mechanisms and discover new therapeutic targets.
Methods: This study utilized RNA sequencing data from multiple public databases, encompassing osteosarcoma samples and healthy controls, along with single-cell RNA sequencing data.
Department of Orthopaedic Surgery, UC Davis Health, Sacramento, CA, USA; Department of Biomedical Engineering, University of California, Davis, CA, USA. Electronic address:
Osteosarcoma (OS), the most common form of primary bone cancer in young adults, has had no improvements in clinical outcomes in 50 years. This highlights a critical need to advance mechanistic understanding of OS to further therapeutic discovery, which will only be possible with accurate models of the disease. Compared to traditional monolayer studies and preclinical models, in vitro models that better replicate the three-dimensional (3D) bone marrow microenvironment will facilitate methodical investigations of the events and factors that drive OS progression.
