| dc.description.abstract | Lung cancer is known as one of the most important causes of death in the world. Today, patients suffering from lung cancer mostly undergo chemotherapy to treat or control lung cancer. Chemotherapy and targeted therapies have significantly improved the prognosis of patients. However, after a successful initial response, some patients relapse when cancer cells become resistant to drug treatment. Unfortunately, due to the severity of the disease and the high use of chemotherapy drugs during the treatment of this type of cancer, most lung cancer patients have drug resistance to drugs, especially Cisplatin. Cisplatin is a known chemotherapeutic agent with excellent clinical effects. The antitumor activity of Cisplatin has been demonstrated in various cancers such as lung cancer. However, resistance of cancer cells to Cisplatin chemotherapy has led to its failure to eradicate cancer cells and subsequent death of cancer patients. Fortunately, much effort has been made to identify the molecular pathways and mechanisms involved in Cisplatin resistance. Studies have shown that altered expression at the level of key genes can accelerate or affect the induction of drug resistance in patients with lung cancer. In recent years, microarray technology and bioinformatics analysis have been widely used to screen for genetic changes at the genome level, allowing us to identify different expressed genes and functional pathways involved in carcinogenesis and progression of lung cancer. has helped.
Materials and Methods: In this study, using data from the Gene Expression Omnibus (GEO) website on gene expression in Cisplatin-resistant lung cancer cell samples, genes with altered expression were identified using R software. Lung cancer A549 cancer cells became resistant to Cisplatin and IC50 of the drug was evaluated at all stages using MTT assay. The expression level of candidate genes was also assessed using qRT-PCR.
Results: After inoculation of lung cancer cells in the laboratory and evaluation of the expression of candidate genes, the results showed that CEACAM1, DGKA, ARHGEF2 and THSD4 genes have altered expression and the IC50 level of Cisplatin in resistant cells is approximately Has increased 11 times. | en_US |
