The biological function and clinical significance of STIL in osteosarcoma

Cancer Cell International

Sheng-Lian Wen¹  Hao Wu²  Pi-wei Huang²  Yu Sun²  Shu-fan Ji³  Mao-lin He³ 

[1] Department of Radiology, The First Affiliated Hospital, Guangxi Medical University, Shuangyong Road 6, 530021, Nanning, Guangxi Zhuang Autonomous Region, People’s Republic of China;Division of Spinal Surgery, The First Affiliated Hospital of Guangxi Medical University, Shuangyong Road 6, 530021, Nanning, Guangxi Zhuang Autonomous Region, People’s Republic of China;Division of Spinal Surgery, The First Affiliated Hospital of Guangxi Medical University, Shuangyong Road 6, 530021, Nanning, Guangxi Zhuang Autonomous Region, People’s Republic of China;Guangxi Collaborative Innovation Center for Biomedicine, Guangxi Medical University, 530021, Nanning, Guangxi Zhuang Autonomous Region, People’s Republic of China;Guangxi-ASEAN Collaborative Innovation Center for Major Disease Prevention and Treatment, Guangxi Medical University, 530021, Nanning, Guangxi Zhuang Autonomous Region, People’s Republic of China;

关键词: STIL;    Osteosarcoma;    Proliferation;    Invasion;    Biomarkers;   

DOI  :  10.1186/s12935-021-01922-y

来源: Springer

【 摘 要 】

BackgroundSCL/TAL1 interrupting locus (STIL) is associated with the progression of several tumors; however, the biological role of STIL in osteosarcoma remains poorly understood.MethodsIn 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.ResultsOsteosarcoma 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.ConclusionsSTIL 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.

【 授权许可】

CC BY