STAT3在非小细胞肺癌耐药中的研究进展

Role of STAT3 in Resistance of Non-small Cell Lung Cancer

近年来,肿瘤炎症微环境对非小细胞肺癌(non-small cell lung cancer, NSCLC)耐药影响的机制研究刚刚起步,信号传导及转录激活因子3(signal transducers and activators of transcription 3, STAT3)作为连接炎症和肿瘤的关键信号通路分子,其活化可引起肿瘤细胞中诸多基因沉默、表达异常及基因的不稳定等,诱导化疗、靶向药物治疗耐药,有望成为潜在的逆转耐药的新靶点。本综述阐述了STAT3在NSCLC获得性耐药中的研究进展,以探讨其作为逆转耐药新靶点的可能性,为NSCLC获得性耐药的临床治疗新策略提供理论依据。

The inflammatory state of tumor microenvironment play an important role in non-small cell lung cancer(NSCLC) drug resistance. As the key signal pathway connecting inflammation and tumor, activated signal transduction and transcriptional activation factor 3(STAT3) leads togenetic abnormal expression, gene silencing, genomic instability, etc. in tumor cells, and induces therapeutic resistance. STAT3 has thepotential to be a new target for reversal of resistance. In this review, we summarize the progress of STAT3 in acquired drug resistance of NSCLC, explore the possibility of STAT3 as a new target to reverse drug resistance, and provide basic theories for the new clinical treatment strategy of acquired drug resistance in NSCLC.