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Background: Osteosarcoma has become the most common bone malignancy in adolescents. Although the clinical treatment of osteosarcoma has advanced considerably in recent years, the 5-year survival rate has not improved significantly. Recently, many studies have shown that mRNA has unique advantages as a target for drug therapy. Therefore, this study aimed to identify a new prognostic factor and provide a new target for the treatment of osteosarcoma to improve the prognosis of patients., Methods and Results: We selected prognostic genes that are closely associated with osteosarcoma clinical features by obtaining osteosarcoma patient information from the GTEx and TARGET databases, and then we developed a risk model. We detected the expression of FKBP11 in osteosarcoma by qRT-PCR, western blotting, and immunohistochemistry and performed CCK-8, Transwell, colony formation, and flow cytometry assays to reveal the regulatory role of FKBP11. We found that FKBP11 was highly expressed in osteosarcoma; silencing FKBP11 expression suppressed the invasion and migration of osteosarcoma cells, slowed cell proliferation, and promoted apoptosis. We also found that silencing the expression of FKBP11 led to inhibition of MEK/ERK phosphorylation., Conclusions: In conclusion, we validated that the prognostic factor FKBP11 is closely associated with osteosarcoma. Additionally, we identified a novel mechanism by which FKBP11 ameliorates the malignant properties of osteosarcoma cells through the MAPK pathway and serves as a prognostic factor in osteosarcoma. This study provides a new method for the treatment of osteosarcoma.

Background: Osteosarcoma (OS) is a common disease in the world, and its pathogenesis is still unclear. This study aims to identify the key genes that promote the proliferation, invasion, and metastasis of osteosarcoma cells., Method: GSE124768 and GSE126209 were downloaded from the Gene Expression Omnibus (GEO) database. The gene ontology and enrichment pathway were analyzed by FunRich software. qPCR and Western blot were used to detect the gene expression. After gene knockdown, Transwell and wound healing assays were conducted on osteosarcoma cells to detect whether the genes were defined before enhancing the invasion of osteosarcoma., Results: Totally, 341 mRNAs were found to be regulated differentially in osteosarcoma cells compared to osteoblasts. In addition, the expression level of Serglycin (SRGN) in osteosarcoma cells was higher than that in human osteoblasts. The invasion and proliferation ability of osteosarcoma cells with upregulated Serglycin was significantly increased, and on the contrary, decreased after Serglycin knockdown. Moreover, we preliminarily found that Serglycin may associate with the JAK/STAT signaling pathway., Conclusions: By using microarray and bioinformatics analyses, differently expressed mRNAs were identified and a complete gene network was constructed. To our knowledge, we describe for the first time Serglycin as a potential biomarker.

Osteosarcoma, a highly aggressive malignant tumor of the bone, usually occurs in children and young adults. However, although the considerable achievement in the clinical treatment of osteosarcoma recent years, the overall survival of osteosarcoma patients has not been obviously improved. Cancer cells preferentially use glycolysis instead of oxidative phosphorylation to meet their increased energetic and biosynthetic demands, a phenomenon known as the Warburg effect. Glycolysis is a driving factor in multiple cancers and is emerging as a new cancer target treatment. In the present study, we established a model to screen for glycolysis-associated genes in osteosarcoma. This risk score of the model were correlated with clinical characteristics osteosarcoma patients. Besides, a functional assay identified that STC2 enhanced the glycolysis of osteosarcoma cells. Modulation of STC2 changes glucose consumption and lactate production as well as GLUT1 expression in osteosarcoma. Furthermore, we identified that change in the expression levels of STC2 affected the proliferation, invasion, and migration of osteosarcoma cells. Our findings showed STC2 as a new tumor-promoting factor of osteosarcoma cells through enhancing glycolysis., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Background: Long noncoding RNAs (LncRNAs) show dysregulation in a variety of cancers. However, the function and specific mechanism of LncRNA GSEC in the progression of osteosarcoma remain mostly unknown. In this study, we sought to elucidate the role and mechanism of LncRNA GSEC in the occurrence and progression of osteosarcoma., Methods: we examined the expression of LncRNA GSEC in osteosarcoma cell lines by quantitative real time PCR. In vitro experiments, including transwell assays, cck8 assays, and flow cytometry analysis have biologically demonstrated the effect of LncRNA GSEC on the proliferation and migration of osteosarcoma cell lines. Furthermore, the regulation of miR-588 by LncRNA GSEC was determined by luciferase reporter assay and quantitative real time PCR. What's more, subcutaneous tumor formation was performed in nude mice to monitor the growth of the tumor in vivo., Results: We found that the expression of LncRNA GSEC was up-regulated in osteosarcoma cell lines. Overexpression of LncRNA GSEC promoted the proliferating and migratory capacity, and inhibited the apoptosis of osteosarcoma cells. Conversely, knockdown of LncRNA GSEC resulted in the opposite effect. Mechanistically, we identified LncRNA GSEC functioned as the sponge of miR-588, thus inhibiting the miR-588/EIF5A2 signal pathway. In addition, the expression of miR-588 was negatively correlated with LncRNA GSEC, and the effect by silencing or overexpressing LncRNA GSEC could be rescued by the introduction of miR-588 mimics or inhibitors, respectively., Conclusions: In summary, this study shows that LncRNA GSEC promotes the proliferation and invasion of OS through the regulation of miR-588/EIF5A2 pathway, which might provide a new strategy for the treatment of osteosarcoma in the future., Competing Interests: Declaration of competing interest None., (Copyright © 2020 Elsevier Inc. All rights reserved.)