ArticleCancer cell international2021
The biological function and clinical significance of STIL in osteosarcoma.
Article in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Multi-omics analysis reveals the key role of STIL in Li-Fraumeni syndrome and osteosarcoma.NPJ precision oncology · 2026Article
- O-GlcNAcylation of NONO regulates paraspeckle component assembly and contributes to colon cancer cell proliferation.Cell death discovery · 2025Article
- Interaction of STIL with FOXM1 regulates SF3A3 transcription in the hepatocellular carcinoma development.Cell division · 2025Article
- Regulatory factor X-5/SCL/TAL1 interruption site axis promotes aerobic glycolysis and hepatocellular carcinoma cell stemness.The Kaohsiung journal of medical sciences · 2025Article
- Telomeres and telomerase in Sarcoma disease and therapy.International journal of medical sciences · 2024Review
- FAM60A promotes osteosarcoma development and progression.Cancer medicine · 2023Article
- Lung Cancer Gene Regulatory Network of Transcription Factors Related to the Hallmarks of Cancer.Current issues in molecular biology · 2023Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
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.
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