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Background: Emerging evidence suggests that secreted phosphoprotein 1 (SPP1) is involved in tumor cell progression in multiple cancer types. However, the role of SPP1 in different cancers is still not clear. Methods:We used data from The Cancer Genome Atlas (TCGA) to analyze the multiomic roles of SPP1, including RNA expression, DNA methylation, protein phosphorylation, immune infiltration, and overall survival (OS) in 33 tumor types.Results: SPP1 is highly expressed in most cancer types, and its methylation variability and mRNA expression level are both correlated with prognosis in multiple cancer types. A higher S234 phosphorylation level was observed in 4 types of tumors, including colon adenocarcinoma (COAD) and lung adenocarcinoma (LUAD). SPP1 expression level was positively associated with the infiltration level of dendritic cells, neutrophils, and macrophages in multiple cancer types. It was also significantly positively correlated with hepatitis A virus cellular receptor 2 (HAVCR2), which was observed in most tumor types, including brain lower grade glioma (LGG) and ovarian serous cystadenocarcinoma (OV). Moreover, myeloid cell differentiation and leukocyte migration were observed in the enrichment analysis, suggesting that SPP1 might induce immune escape.Conclusions: Pan-cancer analysis using a multiomic approach offered a comprehensive overview of SPP1. This protein plays an important role in most of the analyzed tumor types and could be a valuable prognostic marker across different types of cancer.

ObjectivesThe roles played by β-III-spectrin, also known as spectrin beta, non-erythrocytic 2 (SPTBN2), in the occurrence and development of lung adenocarcinoma (LUAD) have not been previously examined. Our study aimed to reveal the relationship between the SPTBN2 expression and LUAD.Materials and MethodsTwenty pairs of LUAD tissues and adjacent tissues were collected from patients diagnosed and treated at the Thoracic Surgery Department of The First Affiliated Hospital of Zhengzhou University from July 2019 to September 2020. RNA sequencing (RNA-seq) analysis determined that the expression of SPTBN2 was higher in LUAD samples than in adjacent normal tissues. The expression levels of SPTBN2 were examined in various databases, including the Cancer Cell Line Encyclopedia (CCLE), Gene Expression Omnibus (GEO), and Human Protein Atlas (HPA). The Search Tool for the Retrieval of Interacting Genes (STRING) online website was used to examine protein–protein interactions involving SPTBN2, and the results were visualized by Cytoscape software. The Molecular Complex Detection (MCODE) plug-in for Cytoscape software was used to identify functional modules of the obtained protein–protein interaction (PPI) network. Gene enrichment analysis was performed, and survival analysis was conducted using the Kaplan–Meier plotter. The online prediction website TargetScan was used to predict SPTBN2-targeted miRNA sequences by searching for SPTBN2 sequences. Finally, we verified the expression of SPTBN2 in the obtained tissue samples using real-time fluorescence quantitative polymerase chain reaction (RT-qPCR). The human lung cancer cell lines A549 and H1299 were selected for the transfection of small interfering RNA (siRNA) targeting SPTBN2 (si-SPTBN2), and the knockdown efficiency was evaluated by RT-qPCR. The cellular proliferation, migration, and invasion capacities of A549 and H1299 cells were determined using the cell counting kit-8 (CCK-8) proliferation assay; the wound-healing assay and the Transwell migration assay; and the Matrigel invasion assay, respectively.ResultsThe expression of SPTBN2 in non–small cell lung cancer (NSCLC) ranked 13th among cancer cell lines based on the CCLE database. At the mRNA and protein levels, the expression levels of SPTBN2 were higher in LUAD tissues than in normal lung tissues. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed that proteins related to SPTBN2 were enriched in apoptotic and phagosomal pathways. Kaplan–Meier survival analysis revealed that SPTBN2 expression was significantly related to the prognosis of patients with LUAD. The TargetScan database verified that miR-16 was a negative regulator of SPTBN2 mRNA expression. The results of the CCK-8 cell proliferation assay revealed that SPTBN2 knockdown significantly inhibited the cell proliferation abilities of A549 and H1299 cells. The wound-healing assay indicated that SPTBN2 knockdown resulted in reduced migration after 48 h compared with the control group. The Transwell migration and invasion test revealed that the migration and invasion abilities were greatly decreased by SPTBN2 knockdown compared with control conditions.ConclusionWe uncovered a novel gene, SPTBN2, that was significantly upregulated in LUAD tissues relative to normal tissue expression. SPTBN2 is highly expressed in LUAD, positively correlated with poor prognosis, and can promote the proliferation, migration, and invasion of LUAD cells.

Background: To explore the risk factors and prevention methods of cervical mechanical anastomotic fistula and stenosis after the radical resection of esophageal cancer. Methods: From March 2018 to November 2018, 128 patients undergoing mechanical anastomosis of esophageal cancer were selected from the