Osteosarcoma transcriptome data exploration reveals STC2 as a novel risk indicator in disease progression

Abstract Background Osteosarcoma has been the most common primary bone malignant tumor in children and adolescents. Despite the considerable improvement in the understanding of genetic events attributing to the rapid development of molecular pathology, the current information is still lacking considering the comprehensive and highly heterogeneous nature of osteosarcoma. The study is to identify more potential responsible genes during the development of osteosarcoma, thus identifying promising gene indicators and aiding more precise interpretation of the disease. Methods Firstly, from GEO database, osteosarcoma transcriptome microarrays were used to screen the abnormally expressed genes (AEGS) in cancer comparing to normal bone samples, followed by GO/KEGG interpretation, risk score assessment and survival analysis of the genes to select a credible key gene. Further, the basic physicochemical properties, predicted cellular location, gene expression in human cancers, association with clinical pathological features and the potential signaling pathways involved in the key gene’s regulation on osteosarcoma development were preliminary explored. Results A total of 24430 genes were identified to express abnormally in osteosarcoma versus normal bone samples, and the genes were classified into four groups based on the difference level, further genes interpretation indicated that the high abnormal level (>8 fold) genes were mainly located extracellular and related to matrix structural constituent regulation. Meanwhile, module function analysis of the 67 high abnormal level (>8 fold) AEGS revealed a 22-gene containing extracellular matrix regulation associated hub gene cluster. Further survival analysis of the 22 genes revealed that STC2 was an independent prognosis indicator in osteosarcoma. Moreover, after the validation of changed expression of STC2 in cancer vs normal tissues using local hospital osteosarcoma samples by IHC experiment, the gene’s physicochemical property revealed STC2 as a cellular stable and hydrophilic protein, and the gene’s association with osteosarcoma clinical pathological parameters, expression in pan-cancers and the probable biological functions and signaling pathways it involved were explored. Conclusions Using multiple bioinformatic analysis and local hospital samples validation, we revealed the aberrant gain of expression of STC2 in osteosarcoma, which associated statistical significantly with patients survival, and the gene’s clinical features and potential biological functions were also explored. Although the results shall provide inspiring insights into further understanding of the disease, further experiments and detailed rigorous clinical trials are needed to reveal its potential drug-target role in clinical medical use.