6-shogaol Targeting HSP60 Induced Apoptosis A549 Non-small Cell Lung Cancer

Objective: NSCLC-resistant target proteins were 6-SH based on molecular biology and chemical biology-related techniques,and their inhibitory effects on A549 cells 6-SH explained from cell,molecular and animal levels respectively.Methods: 1 The value added,invasion,transfer,cycle change and apoptosis of CCK-8 cells were detected by A549,cell scratches,cloning,morphological features and flow cytometry;A A549 cell subcutaneous transplantation tumor model was constructed to observe the effect of 6-SH on tumor growth and metastasis.2 The expression of the apoptotic proteins Bax,Survivin and Bcl-2 was detected by WB 6-SH;JC-1 determination of mitochondrial membrane potential;Network Pharmacological Method Predicts 6-SH Potential Targets and Possible Pathways for Anti-NSCLC;Observation of 6-SH Expression of Key Proteins in PI3K/AKT/m TOR Pathways.3 HPLC-MS/MS was used to identify 6-SH induce A549 apoptosis of key target proteins and validate their mechanism of action;Bioinformatics Database Mining Target Protein Expression Level and Clinical Application.4 CCK-8Method for Determination of Combined Administration of 6-SH and Chemotherapy Drugs Tax,Pt and 5-FU;Toxicity of zebra-fish embryotoxicity by using zebra-fish embryoto.Results: 1 6-SH can significantly inhibit the growth of A549 cells both inside and outside the body;6-SH induces apoptosis and G0/G1 phase block in A549 cells and inhibits A549 cell invasion and transfer.2 6-SH inhibit the expression of Bcl-2 and Survivin protein and promote the expression of Bax protein.6-SH mitochondrial membrane potential decreases,40 corresponding targets 6-SH obtained,KEGG analysis shows that 6-SH corresponding targets participate in a variety of signaling pathways;6-SH suppressed ERK,Stat 3,PI3 K,AKT and m TOR signalling pathways.3 6-SH binds to the HSP60 protein in A549 cells and changes the stability of the HSP60 protein;After NO treatment A549 the sensitivity of cells to 6-SH concentration gradually decreases.4 6-SH and Tax,Pt and 5-FU co-inhibit A549 cell proliferation.Conclusion: 1 6-SH binds to HSP60 in A549 cells and may induce apoptosis by disrupting mitochondrial function.2 The synergies between Tax,Pt,5-FU and 6-SH suggest that 6-SH can be developed as a potential treatment for NSCLC.