拟南芥苷是从白花蛇舌草中提取的，具有明显的抗癌作用。在本研究中，我们探讨了拟南芥苷在非小细胞肺癌细胞（NSCLC）中的抗癌作用和机制。我们的目标是找出拟南芥苷在NSCLC细胞中促进自噬的分子机制。A549和H1299 NSCLC细胞系被用于体外实验。BALB/c裸鼠作为NSCLC动物模型进行了体内实验。 对于体外实验，我们使用CCK-8和EdU试验观察拟南芥苷对NSCLC细胞增殖的影响。利用荧光共聚焦显微镜mCherry-EGFR-LC3试验和电镜试验检测了NSCLC细胞自噬。蛋白质的表达通过Western blot进行检测，mRNA的表达通过qRT-PCR进行检测。流式细胞术用于检测细胞凋亡。对于体内实验，我们使用A549-Luc人类NSCLC细胞系在BALB/C裸鼠中建立皮下移植肿瘤模型。通过测量肿瘤重量和生物发光强度来检测拟南芥苷对NSCLC小鼠模型的影响。免疫组化用于测量小鼠肿瘤组织的关键蛋白质表达。我们的结果确认了拟南芥苷明显抑制了NSCLC细胞的增殖，并促进了NSCLC细胞的自噬，导致了NSCLC细胞的死亡。有趣的是，蛋白质和mRNA水平上的Met都被明显抑制。与此同时，PI3K/AKT/mTOR信号通路也相应被抑制。此外，过表达Met逆转了拟南芥苷对NSCLC细胞存活能力和自噬的影响，具有显著性。最后，我们通过异种移植模型验证了上述的效应和通路。拟南芥苷可能通过促进NSCLC细胞的自噬发挥抗NSCLC作用。在机制上，Met及其下游的PI3K/AKT/mTOR信号通路参与了这个过程，提供了拟南芥苷在抑制NSCLC中的新机制。版权所有 © 2023 Elsevier GmbH。保留所有权利。

Kaempferol is extracted from Hedyotis diffusa, exerting an obvious anti-cancer effect. Here in the present study, we explored the anti-cancer effects and mechanism of kaempferol in non-small cell lung cancer cell (NSCLC).Our objective is to figure out the molecular mechanism by which kaempferol promotes autophagy in NSCLC cells.A549 and H1299 NSCLC cell lines were used for in vitro experiments. And BALB/c nude mice of NSCLC were used to perform in vivo experiments.For in vitro experiments, CCK-8 and EdU assay was used to observe the effect of kaempferol on NSCLC cell proliferation. Confocal microscopy of mCherry-EGFR-LC3 assay and electron microscopy assay were used to detect NSCLC cell autophagy. Protein expression was determined using Western blot, and mRNA expression was determined using qRT-PCR. Flow cytometry was performed to detect the cell apoptosis. For in vivo experiments, a subcutaneously implanted tumor model in BALB/C nude mice was performed using human NSCLC cell line A549-Luc. The kaempferol effect on NSCLC mice model was detected by measuring the tumor weight and bioluminescence intensity. Immunohistochemistry was done to measure the key protein expression from mice tumor tissues.Our results confirmed that kaempferol inhibited NSCLC cell proliferation significantly. And it promoted NSCLC cell autophagy, leading to NSCLC cell death. Interestingly, Met-was greatly inhibited at both protein and mRNA levels. Meanwhile, PI3K/AKT/mTOR signaling pathway was inhibited accordingly. Furthermore, overexpressing Met-reversed the effect of kaempferol on NSCLC cell viability and cell autophagy with significance. Finally, the above effect and pathway were validated using the xenograft model.Kaempferol may exert its anti-NSCLC effect by promoting NSCLC cell autophagy. Mechanistically, Met-and its downstream PI3K/AKT/mTOR signaling pathway were involved in the process, which provides a novel mechanism how kaempferol functions in inhibiting NSCLC.Copyright © 2023 Elsevier GmbH. All rights reserved.