Human ITGB5 ELISA Matched Antibody Pair

Several epithelial-mesenchymal transition (EMT)-associated genes (EAGs) have been confirmed to correlate with the prognosis of hepatocellular carcinoma (HCC) patients. Herein, we explored the value of EAGs in the prognosis of HCC relying on data from The Cancer Genome Atlas (TCGA) database. A total of 200 EMT-associated genes were downloaded from the Gene set enrichment analysis (GSEA) website. Moreover, 96 differentially expressed EAGs were identified. Using Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, we forecasted the potential molecular mechanisms of EAGs. To identify prognostic EAGs, Cox regression was used in developing a prognostic risk model. Then, the Kaplan-Meier and receiver operating characteristic (ROC) curves were plotted to validate the prognostic significance of the model. A total of 5 prognostic correlated EAGs (P3H1, SPP1, MMP1, LGALS1, and ITGB5) were screened via Cox regression, which provided the basis for developing a novel prognostic risk model. Based on the risk model, patients were subdivided into high-risk and low-risk groups. The overall survival of the low-risk group was better compared to the high-risk group (P < 0.00001). The ROC curve of the risk model showed a higher AUC (Area under Curve) (AUC = 0.723) compared to other clinical features (AUC <= 0.511). A nomogram based on this model was constructed to predict the 1-year, 2-year, and 3-year overall survival rates (OS) of patients. Conclusively, we developed a novel HCC prognostic risk model based on the expression of EAGs, which help advance the prognostic management of HCC patients.

Cancer cells harbor lower energy consumption after rounds of anticancer drugs, but the underlying mechanism remains unclear. In this study, we investigated metabolic alterations in cancer cells exposed to cisplatin. The present study exhibited cisplatin, known as a chemotherapeutic agent interacting with DNA, also acted as an anti-metabolic agent. We found that glycolysis levels of breast and cervical cancer cells were reduced after cisplatin treatment, resulting in cells growth and proliferation inhibition. We demonstrated that cisplatin suppressed glycolysis-related proteins expression, including glucose transporter 1 (GLUT1), glucose transporter 4 (GLUT4) and lactate dehydrogenase B (LDHB), through down-regulating integrin beta 5 (ITGB5)/focal adhesion kinase (FAK) signaling pathway. ITGB5 overexpression rescued cisplatin-induced inhibition of cancer cell glycolysis, growth and proliferation. Conclusively, we reveal a novel insight into cisplatin-induced anticancer mechanism, suggesting alternative strategies to the current therapeutic approaches of targeting ITGB5, as well as of a combination of cisplatin with glucose up-regulation chemotherapeutic agents to enhance anticancer effect.