Cancer-associated fibroblasts (CAFs) play a pivotal role in cancer progression; however, how CAFs are induced remains elusive. Sulfonylurea receptor 1 (SUR1) is a tumor-enhancer in non-small cell lung carcinoma (NSCLC). Here, we probed the influence of SUR1-expressing cancer cells on CAFs.
View Article and Find Full Text PDFBackground: The third-generation epithelial growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) have shown significant therapeutic effects on patients with non-small cell lung carcinoma (NSCLC) who carry active EGFR mutations, as well as those who have developed acquired resistance to the first-generation of EGFR-TKIs due to the T790M mutation. However, most patients develop drug resistance after 8-10 months of treatment. Currently, the mechanism has not been well clarified, and new therapeutic strategies are urgently needed.
View Article and Find Full Text PDFAEG-1 has been proven to be tumor enhancer in gastric cancer. However, its mechanism has not yet been fully clarified. Gain-of-function and loss-of-function experiments were conducted to determine the role of eIF4E in AEG-1-induced growth of gastric cancer cells and xenografts of a nude mouse model.
View Article and Find Full Text PDFSulfonylurea receptor 1 (SUR1) is the regulatory subunit of ATP-sensitive potassium channels (K channels) and the receptor of antidiabetic drugs, such as glibenclamide, which induce insulin secretion in pancreatic β cells. However, the expression and role of SUR1 in cancer are unknown. In this study, we found that SUR1 expression was elevated in human non-small cell lung carcinoma (NSCLC) tissues and cell lines.
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