由于化疗药物存在副作用强和引发耐药性问题,故研发高效抗癌药物是征服肺癌所面临的迫切要求。课题组前期研究发现：LL-37衍生抗菌肽merecidin可能通过细胞凋亡途径抑制非小细胞肺癌A549细胞的生长，且merecidin作用于A549细胞后JNK信号通路的相关基因的表达差异大，故我们提出假说：抗菌肽merecidin通过JNK信号通路介导细胞凋亡并影响细胞自噬，为证明该假说特设计以下实验：首先通过WB等系列实验证明抗菌肽是通过JNK信号通路介导细胞凋亡和自噬，其次分别利用慢病毒系统和CRISP/Cas9技术过表达及敲除JNK信号通路中关键的基因JNK，观察在过表达和敲除之后JNK信号通路下游基因和蛋白表达的变化情况，最后通过动物实验研究抗菌肽抑制移植瘤模型裸鼠的肿瘤生长情况。通过上述分子、细胞、动物实验，详细阐述merecidin通过JNK信号途径在细胞凋亡和自噬过程中的作用机制。

As the side effects and resistance of chemotherapy drugs, so the development of highly effective drugs to conquer lung cancer is urgently. Through the previous study of our group has found: Antimicrobial peptide merecidin which derived by LL-37 inhibits the growth of non-small cell lung cancer A549 through the apoptotic pathway. Furtherly, we found that the expression of JNK signaling pathway was significantly different when merecidin was acted on A549. So we put forward the hypothesis: Through the JNK signaling pathway, apoptosis and autophagy was caused by antimicrobial peptide merecidin. In order to prove this hypothesis we designed the following experiment: First, Western-Blot and other series of experiments were used to demonstrate that apoptosis and autophagy were mediated by antimicrobial peptides through the JNK signaling pathway. The second step is to observe the changes in the downstream genes and protein expression when overexpressed and knocked out the key genes in the JNK signaling pathway. To achieve this goal, lentivirus systems and CRISP / CAS9 overexpression techniques were used separately. Finally, animal experiments were conducted to study the effect of antimicrobial peptides on tumor growth in nude mice transplanted tumor model. Using molecular, cellular and animal experiments in the above, the mechanisms of apoptosis and autophagy caused by merecidin through the JNK signaling pathway is described in detail.