Identification of Notch signaling pathway gene mutations as a prognostic biomarker for bladder cancer

Purpose: The authors aimed to identify Notch signaling pathway gene mutations as a prognostic biomarker for bladder cancer. Methods: First, critical Notch signaling pathway genes were screened using The Cancer Genome Atlas and validation sets. Second, immune infiltration, protein–protein interaction network, Kyoto Encyclopedia of Genes and Genomes and Gene Set Enrichment Analysis analyses were performed. Finally, potential immunotherapy drug targets were screened using T-cell receptors, B-cell receptors and CERES scores for bladder cancer. Results: The NOTCH7 gene was identified, with a significant difference in immune infiltration level between mutant and wild type in bladder cancer, mainly related to T cells. NOTCH7 was an immunotherapy prognostic factor, and IRF1 and B2M were the potential drug targets for NOTCH7 mutation in bladder cancer. Conclusion: NOTCH7 gene mutation can be used as an immunotherapy biomarker for bladder cancer.

Autogenous and anautogenous Culex pipiens bioforms exhibit insulin-like peptide signaling pathway gene expression differences that are not dependent upon larval nutrition

Culex pipiens form pipiens and Cx. pipiens form molestus differ in their ability to produce eggs without a bloodmeal. Autogenous mosquitoes, such as the molestus bioform of Cx. pipiens, depend on nutrition acquired as larvae instead of a bloodmeal to fuel the energy intensive process of vitellogenesis, which requires abundant production of yolk proteins. In anautogenous mosquito systems, ovary ecdysteroidogenic hormone (OEH) and insulin-like peptides (ILPs) transduce nutritional signals and trigger egg maturation in response to a bloodmeal. It is unclear to what extent the process is conserved in autogenous mosquitoes and how the bloodmeal trigger has been replaced by teneral reserves. Here, we measured the effects of a series of nutritional regimens on autogeny, time to pupation, and survival in Cx. pipiens form molestus and form pipiens. We find that abundant nutrients never result in autogenous form pipiens and extremely poor food availability rarely eliminates autogeny from form molestus. However, the number of autogenous eggs generated increases with nutrient availability. Similarly, using qPCR to quantify gene expression, we find several differences in the expression levels of ilps between bioforms that are reduced and delayed by poor nutrition, but not extinguished. Changes in OEH expression do not explain bioform-specific differences in autogeny. Surprisingly, the source of most of the gene expression differences correlated with autogeny is the abdomen, not the brain. Overall, our results suggest that autogeny is modulated by nutritional availability, but the trait is encoded by genetic differences between forms and these impact the expression of ILPs.

Research Progress on Slit/Robo Pathway in Pancreatic Cancer: Emerging and Promising

Pancreatic cancer is a highly malignant digestive system tumor which is the leading cause of cancer-related deaths. The basic and clinical research of pancreatic cancer has made great progress in recent years, and kinds of signaling pathways have been found in the tumorigenesis and progression in pancreatic cancer. The Slit glycoprotein (Slit) and Roundabout receptor (Robo) signaling pathway acts as a neural targeting factor with the axonal remnant, axon guidance, and inhibition of neuronal migration in the nervous system. In recent years, it has been found that the Slit/Robo signaling pathway has different degrees of expression changes in various tumor cells. In different tumor cells, the signaling pathway gene expression is different and regulates tumor angiogenesis, cell invasion, metastasis, and nerve infiltration. Herein, we summarize the mechanisms of the Slit/Robo pathway in the development and progression of pancreatic cancer, in order to have more understanding of the role of Slit/Robo in pancreatic cancer.