The effect and mechanism of AKT protein kinase activation on the biological behavior of Caki-2 cells

Objective: To investigate the effects and mechanisms of Protein Kinase B (AKT) activation on the biological behavior of malignant B-cells. Methods: This study used immunohistochemical staining to detect the differences between AKT tumor tissue and short and fat tissue. The RCC cell line Caki-2 was screened using real-time fluorescence quantitative PCR detection and Western blot assay. Analyze the effect of AKT activation on cell adhesion and migration through biomechanical experiments.in order to select the best siRNA experimental group. The effects of CCK8, the Transwell invasion experiment, and flow cytometry on Caki cell proliferation, invasion, migration, apoptosis, and cell cycle were detected. Results: According to the immunohistochemical staining results, it was found that compared to the surrounding normal tissues, AKT1 was expressed higher in tumor tissues (P < 0.05). After AKT activation, it can affect cell adhesion and regulate the function of integrins by phosphorylating various substrates. Integrins are cell adhesion molecules that can mediate cell adhesion to the extracellular matrix. AKT can enhance the adhesion between cells and matrix by phosphorylating integrins or their related signaling molecules. After AKT activation, it can promote the migration and invasion ability of cells. This is mainly achieved by activating multiple signaling pathways, such as Rac and Rho family proteins. These signaling pathways play important roles in cytoskeleton remodeling and cell movement. Phosphorylated AKT can activate these pathways, thereby promoting cell migration. AKT activation in Caki-2 cells via siRNA transfection demonstrated that AKT activation promoted the proliferation, invasion, After Caki-2 cell migration, AKT can transition Caki-2 cells from the G1 phase to the S phase. Conclusion: AKT may be involved in the malignant growth of RCC and holds potential as a therapeutic target.