Abstract
BackgroundThyroid cancer (TC) is the most common endocrine malignancy; basigin (also known as BSG) plays a crucial role in tumor cell invasion, metastasis, and angiogenesis. This study was designed to identify the change of BSG expression in TC and its possible potential mechanism.MethodsThe BSG expression levels in TC were demonstrated using data collected from in-house immunohistochemical (IHC), RNA-sequencing (RNA-seq), microarrays, and literatures. Integrated analysis was performed to determined BSG expression levels in TC comprehensively. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed with the integration of BSG co-expressed genes and differentially expressed genes (DEGs) in TC tissues to explore the potential mechanisms of BSG in TC.ResultsThe protein expression level of BSG was significantly higher in TC cases based on the IHC experiments. In addition, the combined SMD for BSG expression was 0.39 (p < 0.0001), the diagnostic odds ratio was 3.69, and the AUC of the sROC curve was 0.6986 using 1182 TC cases and 437 non-cancerous cases from 17 independent datasets. Furthermore, BSG co-expressed genes tended to be enriched in gene terms of the extracellular matrix (ECM), cell adhesion, and cell-cell interactions. The expression levels of nine hub BSG co-expressed genes were markedly upregulated in TC cases.ConclusionBSG expression levels were closely correlated with the progression of TC and may affect the signals of the ECM, cell adhesion, and cell-cell interactions.
Highlights
Thyroid cancer (TC) is the most common endocrine malignancy; basigin plays a crucial role in tumor cell invasion, metastasis, and angiogenesis
The area under the curve (AUC) of BSG protein expression used to distinguish between TC cases and non-cancerous cases was 0.985 (95%confidence interval (CI) 0.971 to 0.999, p < 0.0001)
Hub genes of BSG in TC Using Proteinprotein interaction (PPI) analysis and CytoHubba, we identified the top genes as hub genes of BSG in TC (Fig. 8k): cyclin dependent kinase 1 (CDK1), kinesin family member (KIF11), topoisomerase (DNA) II alpha (TOP2A), ribonucleotide reductase regulatory subunit M2 (RRM2), microtubule nucleation factor (TPX2), PDZ binding kinase (PBK), maternal embryonic leucine zipper kinase (MELK), DLG-associated protein 5 (DLGAP5), kinetochore complex component (NDC80), and nucleolar and spindle associated protein 1 (NUSAP1)
Summary
Thyroid cancer (TC) is the most common endocrine malignancy; basigin ( known as BSG) plays a crucial role in tumor cell invasion, metastasis, and angiogenesis. This study was designed to identify the change of BSG expression in TC and its possible potential mechanism. Recent studies have confirmed a few molecular markers that have allowed better understanding of the molecular mechanisms of TC, for instance, BRAF and RAS point mutations, RET/PTC and PAX8/PPAR gene rearrangements, etc [5,6,7]. The latest study found that Substance P/neurokinin-1 receptor (SP/NK-1R) system was over-expressed in TC than that in normal thyroid tissues via immunohistochemical study, which could promote the migration and invasion of cancer cells [8]. It was critical to continue to study the molecular mechanisms involved in TC, which may provide new strategies for the diagnosis and treatment of TC patients in the future
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