Methods: The posterior parts of the archwires were sectioned into 20 mm segments (N = 102) and divided among six groups. Four groups were treated with different pH levels and two served as controls. The specimens were immersed in individual test tubes containing 10 ml of artificial saliva adjusted to a pH of 6.75 or 3.5. The tubes were sealed and stored in a 37 °C water bath for 28 days. After 28 days, the specimens were ligated to brackets embedded in an acrylic block and subjected to mechanical stress using an electronic toothbrush for 210 s. The specimens were photographed, and images were measured for coating loss using AutoCAD® software. Surface morphology was observed using a scanning electron microscope (SEM).
Results: Significant coating loss (p
MATERIALS AND METHODS: The STIM1 effect was assessed via dicersubstrate siRNA-mediated STIM1 knockdown. The effect of STIM1 knockdown on the expression of AKT and MAPK pathway-related genes and reactive oxygen species (ROS) generation-related genes was tested using real-time polymerase chain reaction. Cellular functions, including ROS generation, cell proliferation, and colony formation, were also evaluated following STIM1 knockdown.
RESULTS: The findings revealed that STIM1 knockdown reduced intracellular ROS levels via downregulation of NOX2 and PKC. These findings were associated with the downregulation of AKT, KRAS, MAPK, and CMYC. BCL2 was also downregulated, while BAX was upregulated following STIM1 knockdown. Furthermore, STIM1 knockdown reduced THP-1 cell proliferation and colony formation.
CONCLUSION: This study has demonstrated the role of STIM1 in promoting AML cell proliferation and survival through enhanced ROS generation and regulation of AKT/MAPK-related pathways. These findings may help establish STIM1 as a potential therapeutic target for AML treatment.