| In recent years,the incidence and mortality of lung cancer in male patients accounted for the first place in malignant tumors.Among female patients,lung cancer incidence and mortality were second only to breast cancer.Lung cancer is divided into non-small cell lung cancer(about 85% of lung cancer)and small cell lung cancer.Currently,the treatment of lung cancer is mainly surgical resection and radiotherapy and chemotherapy.Patients who use chemotherapy drugs for a long time will have different degrees of resistance.Paclitaxel is a first-line chemotherapy drug used clinically.In this study,paclitaxel was used as a drug,and non-small cell lung cancer A549 was used as a cell model to identify biological targets related to drug resistance in non-small cell lung cancer.In this study,human lung adenocarcinoma cell line A549 was used as a control group,and a successful paclitaxel-resistant A549 T was used as an experimental group for methylation chip analysis.After obtaining relevant data,the article used P-Value and Beta-difference as selection criteria.The resulting gene data were screened and 8 genes(KANK1,ALDH3A1,CDKN2 A,GALNT14,PIK3R3,LRG1,RGS20 and WEE2)with greater differences in methylation were selected for subsequent validation.After q RT-PCR expression tests showed that the differential changes in the methylation of these genes were negatively correlated with their expression levels.In this study,the KANK1 gene was finally selected for gene function verification.After interference and apoptosis analysis,the hypomethylation of this gene will make A549 cells more sensitive to paclitaxel and increase cancer cell apoptosis.Therefore,the study concluded that the methylation status of KANK1 gene plays an important role in paclitaxel acquired resistance in human lung adenocarcinoma cell line A549.Through the study,we found the new target molecule KANK1,which provides an experimental basis for clinical drug resistance treatment. |