The Mechanism Of Daidzein Induced Human Lung Cancer A549 Cells Apoptosis

Lung cancer is a malignancy disease that threaten human’s health around the world.Cancer data analysis shows that about 1.76 million tumor patients die from lung cancer each year.Daidzein(DAI)is a kind of natural isoflavone compound in soybean products,and it has been brought into focus the scholars from all over the world because of its good pharmacological mechanism of pharmacodynamics,but its anti-cancer mechanism for lung cancer is still not clear.Therefore,in this study,lung cancer cells were used as an in vitro study model to study the anticancer mechanism of DAI from the cellular and molecular levels.In this experiment,to detected the killing effect of DAI on three lung cancer cells and the toxic effects on three normal cells,the Cell Counting Kit-8 method was used for detection;Fluorescence microscopy and flow cytometry(FCM)were used to detect the apoptosis induced by DAI;With the method of FCM to detecte the cycle arrest effect of DAI in lung cancer cells;FCM is also suitable for detecting the regulation effect of DAI on reactive oxygen species(ROS)in human lung cancer cells;The inhibitory effect of DAI on the migration of lung cancer cells was detected by cell scratch test;Through western blot to detect cell apoptosis,ROS levels,cycle arrest,migration inhibition and protein expression levels of related signaling pathways.The results showed that compared with the positive control 5-FU group,DAI had a killing effect on three lung cancer cells,and showed no significant toxic side effects on three normal cells;As the time of DAI treating A549 cells increased,the apoptotic morphology of A549 cells was obviously wrinkled and rounded,the sum of the number of early and late apoptotic cells was continuously increased,and the mitochondrial membrane potential in A549 cells was significantly decreased.In addition,DAI could also significantly reduce the ratio of apoptosis-related protein Bcl-2/Bad,release Cytochrome C,and mediates the activation of caspase-3 and PARP,and finally leads to mitochondria-dependent apoptosis;DAI can induce cycle arrest in G0/G1 phase by promoting the expression of p21 and p27 and inhibiting the expression of p-Akt,CDK2/4/6 and cyclin D1/E;DAI can up-regulate ROS level in lung cancer A549 cells,to activate JNK and p38 signaling pathways,to inhibit ERK,STAT3 and NF-κB signaling pathways,and to induce apoptosis of A549 cells;After treatment with DAI,the migration of A549 cells was significantly inhibited in a time-dependent manner,and the migration of A549 lung cancer cells was effectively inhibited by TGF-β signaling pathway.Combined with the above results,DAI can kill three lung cancer cells,and increase the ROS level in lung cancer A549 cells,further influence the regulation of the MAPK,STAT3 and NF-κB signaling pathways,to induce mitochondria-dependent apoptosis and cell cycle arrest in lung cancer A549 cells,also inhibit cell migration and invasion by regulating TGF-β signaling pathway.This study provides a new idea and theoretical basis for the development of a safe and effective prevention and treatment of tumor functional factor.