白介素37下调多药耐药基因-1逆转肺腺癌紫杉醇耐药的研究  

Study on interleukin⁃37 downregulating multidrug resistance gene⁃1 to reverse paclitaxel resistance in lung adenocarcinoma

作　　者：王梦馨 陈文 李晨瑜 李志文 牟晓峰[3] WANG Mengxin;CHEN Wen;LI Chenyu;LI Zhiwen;MU Xiaofeng(Medical College of Qingdao University,Qingdao,Shandong,China,266001;Department of Hyperbar-ic Oxygen,Affiliated Qingdao Central Hospital of Qingdao University,Qingdao Cancer Hospital,Qingdao,Shandong,China,266000;Department of Laboratory Medicine,Affiliated Qingdao Central Hospital of Qingdao University,Qingdao Cancer Hospital,Qingdao,Shandong,China,266000)

机构地区：[1]青岛大学医学部,山东青岛266001 [2]青岛大学附属青岛市中心医院,青岛市肿瘤医院高压氧科,山东青岛266000 [3]青岛大学附属青岛市中心医院,青岛市肿瘤医院检验科,山东青岛266000

出　　处：《分子诊断与治疗杂志》2024年第5期979-984,共6页Journal of Molecular Diagnostics and Therapy

摘　　要：目的 本研究旨在探究白介素37(IL-37)在抑制肺腺癌细胞多药耐药性方面的潜在作用,及其对于耐紫杉醇的A549/TAX细胞的影响。方法 通过细胞培养、处理程序、实时荧光定量PCR、Western blot分析和统计学分析等实验方法,系统研究了IL-37对耐紫杉醇A549/TAX细胞的影响。结果 紫杉醇明显抑制了A549和A549/TAX细胞的增殖,其中A549/TAX的耐药指数RI为16.88。100ng/mL的rhIL-37显著抑制了A549/TAX细胞的增殖。在紫杉醇和rhIL-37联合处理组,细胞增殖的抑制率显著高于仅用紫杉醇处理组(P<0.05)。此外,rhIL-37在24小时后显著抑制了A549/TAX细胞的迁移和侵袭。非细胞毒性浓度的rhIL-37也能显著抑制A549/TAX细胞的集落形成。经rhIL-37作用48小时后,A549/TAX细胞中MDR1的表达水平比对照组下降了约66%(P<0.05)。结论 IL-37与紫杉醇联合处理可有效抑制A549/TAX细胞的增殖、迁移和侵袭,同时通过降低MDR1基因的表达水平可能逆转细胞的耐药性,为IL-37在肺腺癌治疗中的潜在应用提供了实验依据。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 proliferation,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.

关 键 词：白介素37 紫杉醇耐药 非小细胞肺癌 多药耐药基因-1 

分 类 号：R734.2[医药卫生—肿瘤]