Study on interleukin-37 downregulating multidrug resistance gene-1 to reverse paclitaxel resistance in lung adenocarcinoma
Objective To explore the potential role of interleukin-37(IL-37)in inhibiting multi-drug resistance(MDR)in lung adenocarcinoma cells and its impact on paclitaxel-resistant A549/TAX cells.Methods Using cell culture,treatment protocols,real-time fluorescence quantitative PCR,Western blot analysis,and statistical analysis,the effects of IL-37 on paclitaxel-resistant A549/TAX cells were systematical-ly studied.Results Paclitaxel significantly inhibited the proliferation of both A549 and A549/TAX cells,with the resistance index(RI)for A549/TAX being 16.88.At a concentration of 100 ng/mL,rhIL-37 significantly suppressed A549/TAX cell proliferation.The combination of paclitaxel and rhIL-37 showed a significantly higher inhibition rate of cell proliferation compared to paclitaxel alone(P<0.05).Additionally,rhIL-37 mark-edly inhibited the migration and invasion of A549/TAX cells after 24 hours.Non-cytotoxic concentrations of rhIL-37 also significantly suppressed colony formation of A549/TAX cells.After 48 hours of rhIL-37 treat-ment,the expression level of MDR1 in A549/TAX cells decreased by approximately 66%compared to the con-trol group(P<0.05).Conclusion Combining IL-37 and paclitaxel treatment can effectively inhibit the prolif-eration,migration,and invasion of A549/TAX cells.By reducing the expression level of the MDR1 gene,it may reverse the cell's drug resistance,providing experimental evidence for the potential application of IL-37 in the treatment of lung adenocarcinoma.
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