Neurotensin receptor 1 (NTSR1) is linked with poor prognosis in many tumors, including gastric cancer (GC). However, the exact mechanism by which NTSR1 affects GC anoikis in GC has not yet been clarified. Therefore, this project aimed to figure out the specific mechanism by which NTSR1 participated in GC anoikis. We herein assessed the expression of KLF5 and NTSR1 in GC tissues and the signaling pathways in which NTSR1 participated through the online bioinformatics website. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was employed to examine the expression of KLF5 and NTSR1. The CCK-8 kit was applied to detect the viability of GC cells under different treatments. Dual luciferase and chromatin immunoprecipitation (ChIP) experiments verified the binding relationship between KLF5 and NTSR1. The rate of fatty acid oxidation (FAO) was analyzed using a cell metabolism meter. The expression of FAO-related proteins was detected using the western blot (WB). The anoikis of cells in each group was detected using flow cytometry, anoikis apoptosis kit, and WB. We observed that knocking down NTSR1 repressed the vitality of GC cells, and elevated the anoikis rate and the expression of cleaved PARP and cleaved caspase 3 in GC cells. Moreover, high expression of NTSR1 up-regulated the expression of CTP1 protein in FAO and increased FAO levels, thereby suppressing the occurrence of anoikis in GC cells. The addition of the inhibitor of FAO (Etomoxir) reversed the above trends. In addition, KLF5 was highly expressed in GC, and KLF5 is an upstream transcription factor of NTSR1. Finally, KLF5 knockdown was verified to restore the repression of the FAO pathway and facilitate anoikis in GC cells by overexpressing NTSR1. In summary, our results suggested that KLF5 affects anoikis in GC cells by targeting NTSR1 to modulate the FAO pathway. Therefore, blocking the FAO pathway regulated by the KLF5/NTSR1 axis may become a new strategy for the treatment of GC.

Cold acclimation, defined as gradual habituation to low temperatures by exposure to mild cold temperatures for several days, has been known to enhance an organism's cold tolerance and facilitate its adaptation to seasonal temperature changes in temperate regions. The present study focuses on the evolution of the cold acclimation response in Drosophila albomicans, which rapidly expanded its distribution from tropical Southeast Asia to Japanese main islands in the mid-1980s. This research aims to elucidate the genetic mechanisms underlying cold acclimation through gene expression changes. The gene expression changes due to cold acclimation were compared among five strains with different genetic backgrounds to identify the genes involved in these processes. High-throughput mRNA sequencing (RNA-seq) was employed to identify differentially expressed genes (DEGs) in strains from China, Taiwan, and Japan under cold acclimation and control conditions. The results suggest that the actin genes play a critical role in cellular functions at low temperatures. A reduction in the expression of mElo is likely to result in decreased levels of C18 fatty acids, thereby enhancing cellular cold tolerance. Furthermore, this study highlights the universality and diversity of gene expression changes in response to cold acclimation. While many DEGs shared by all five strains were the genes involved in metabolic pathways, many strain-specific DEGs were the genes involved in gene regulation. This suggests that the genes with critical roles in fundamental cellular and physiological processes are subject to evolutionary constraints, and that the genes involved in regulatory functions or responding to local environmental conditions may undergo rapid evolution to exhibit significant variability. These results provide insight into the genetic mechanisms of environmental adaptation and population expansion in nature.