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Updated: Nov 9, 2025
Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma
Published on: April 12, 2019
The biological function and clinical significance of STIL in osteosarcoma
Shu-Fan Ji1,2,3, Sheng-Lian Wen4, Yu Sun1
1Division of Spinal Surgery, The First Affiliated Hospital of Guangxi Medical University, Shuangyong Road 6, Nanning, 530021, Guangxi Zhuang Autonomous Region, People's Republic of China.
Background:
SCL/TAL1 interrupting locus (STIL) is associated with the progression of several tumors; however, the biological role of STIL in osteosarcoma remains poorly understood.
Methods:
In this study, the clinical significance of STIL in osteosarcoma was analyzed by gene chip data recorded in public databases. STIL expression was silenced in osteosarcoma cell lines to observe the effects on proliferation, apoptosis, invasion, and migration. Differentially expressed genes (DEGs) in the osteosarcoma chip were analyzed using The Limma package, and STIL co-expressed genes were obtained via the Pearson correlation coefficient. The potential molecular mechanism of STIL in osteosarcoma was further explored by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways.
Results:
Osteosarcoma was associated with higher STIL expression compared to the control samples, and the standardized mean difference (SMD) was 1.52. STIL also had a good ability to distinguish osteosarcoma from non-osteosarcoma samples [area under the curve (AUC) = 0.96]. After silencing STIL, osteosarcoma cell proliferation decreased, apoptosis increased, and the migratory and invasion ability decreased. A total of 294 STIL differentially co-expressed genes were screened, and a bioinformatics analysis found that differentially co-expressed genes were primarily enriched in the cell signaling pathways. The protein-protein interaction (PPI) network indicated that the hub differentially co-expressed genes of STIL were CDK1, CCNB2, CDC20, CCNA2, BUB1, and AURKB.
Conclusions:
STIL is associated with osteosarcoma proliferation and invasion, and may be promote the progression of osteosarcoma by regulating the expression of CDK1, CCNB2, CDC20, CCNA2, BUB1 and AURKB.
Insights
STIL gene expression is elevated in osteosarcoma, promoting tumor progression. Silencing STIL inhibits osteosarcoma cell proliferation and invasion, suggesting STIL as a therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- The SCL/TAL1 interrupting locus (STIL) gene's role in osteosarcoma progression is largely unknown.
- STIL is implicated in the advancement of various other cancers.
Purpose of the Study:
- To investigate the clinical significance and biological function of STIL in osteosarcoma.
- To elucidate the molecular mechanisms underlying STIL's role in osteosarcoma.
Main Methods:
- Analysis of STIL expression in osteosarcoma using public gene chip data.
- In vitro experiments involving STIL gene silencing in osteosarcoma cell lines.
- Bioinformatic analyses including differential gene expression, pathway enrichment (GO, KEGG), and protein-protein interaction network construction.
Main Results:
- Osteosarcoma tissues exhibit significantly higher STIL expression compared to controls (SMD=1.52, AUC=0.96).
- STIL silencing reduced osteosarcoma cell proliferation and invasion while increasing apoptosis.
- STIL co-expression analysis identified 294 differentially expressed genes, primarily involved in cell signaling pathways, with CDK1, CCNB2, CDC20, CCNA2, BUB1, and AURKB identified as key hub genes.
Conclusions:
- STIL expression is correlated with increased proliferation and invasion in osteosarcoma.
- STIL may drive osteosarcoma progression by regulating key cell cycle genes such as CDK1, CCNB2, CDC20, CCNA2, BUB1, and AURKB.
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