由于死亡率增加，非小细胞肺癌（NSCLC）已成为全球可怕的肺癌之一。在化疗方面，吉非替尼已被用作非小细胞肺癌的有效一线治疗药物。尽管如此，对吉非替尼的获得性耐药仍然是NSCLC的治疗障碍之一，需要提高吉非替尼的治疗效果。最初，进行了逆转录定量聚合酶链反应（RT-qPCR）和蛋白质印迹（WB）分析测量临床样本中的微核糖核酸（miRNA，特别是 miR-578）和细胞因子信号传导抑制因子 2 (SOCS2) 水平。此外，体外建立的对吉非替尼耐药的 NSCLC 细胞系通过 miR-578 抑制剂、miR-578 模拟物和 si-SOCS2 转染。同样，构建体内异种移植小鼠模型来验证 miR-578 的逆转作用。我们的研究结果表明吉非替尼耐药组中 miR-578 表达水平增加。此外，抑制 miR-578 表达可显着逆转吉非替尼耐药性。此外，miR-578 的作用是通过 SOCS2 表达水平来调节的。 miR-578降低吉非替尼耐药的作用通过抑制SOCS2表达而减弱。这些研究结果表明，miR-578在体外和体内通过调节NSCLC细胞内SOCS2的表达有效消除吉非替尼耐药。总之，这些结果无疑将为治疗 NSCLC 患者提供潜在的分子治疗靶点和临床治疗提供参考。© 2023 Wiley periodicals LLC。

Nonsmall-cell lung cancer (NSCLC) has emerged as one of the dreadful lung cancers globally due to its increased mortality rates. Concerning chemotherapy, gefitinib has been employed as an effective first-line treatment drug for NSCLC. Nonetheless, the acquired resistance to gefitinib has remained one of the treatment obstacles of NSCLC, requiring improvement in the therapeutic effect of gefitinib.Initially, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and Western blotting (WB) analyses were conducted to measure micro-ribose nucleic acid (miRNA, specifically miR-578) and suppressor of cytokine signaling 2 (SOCS2) levels in the clinical samples. Further, NSCLC cell lines resistance to gefitinib, established in vitro, were transfected by miR-578 inhibitor, miR-578 mimic, and si-SOCS2. Similarly, the xenograft mouse model in vivo was constructed to validate the reversing effect of miR-578.Our findings indicated the increased miR-578 expression levels in the gefitinib resistance group. Further, inhibiting the miR-578 expression substantially reversed the gefitinib resistance. In addition, the miR-578 effect was modulated via the SOCS2 expression level. The decreased gefitinib resistance effect of miR-578 was weakened by inhibiting the SOCS2 expression.These findings demonstrated that miR-578 effectively abolished gefitinib resistance by regulating the SOCS2 expression within NSCLC cells in vitro and in vivo. Together, these results will undoubtedly support a reference to provide potential molecular therapeutic targets and clinical treatments for treating NSCLC patients.© 2023 Wiley Periodicals LLC.