化疗耐药是晚期非小细胞肺癌（NSCLC）生存率低的主要原因之一。长链非编码RNA在NSCLC患者化疗耐药及预后中发挥着重要的作用，但其机制尚不清楚。我们前期研究发现：①LINC00663可促进NSCLC化疗耐药，而高表达miR-194-3P能够降低LINC00663诱导的耐药性；②青蒿素B可靶向抑制NSCLC细胞中LINC00663的表达水平，并提高NSCLC细胞化疗敏感性。基于此，我们提出如下假说：青蒿素B通过调控LINC00663互补“吸附”miR-194-3p的功能，减弱下游靶基因转录后的抑制作用，使下游相关信号通路激活，从而降低NSCLC细胞的化疗耐药性。为确认此假说，我们拟通过系统研究回答青蒿素B、LINC00663、miR-194-3p及下游靶基因对NSCLC化疗耐药调控网络和分子机理之科学问题。本项目可为青蒿素B作为抗肿瘤药治疗晚期NSCLC化疗耐药提供新思路和科学依据。

High incidence of chemotherapy resistance is one of the main reasons for the low survival rate of advanced non-small cell lung cancer (NSCLC). Long non-coding RNA plays an important role in chemotherapy resistance and prognosis of NSCLC patients, but the mechanism is still unclear. Our previous research found that: ①LINC00663 could promote chemotherapy resistance in NSCLC, and high expression of miR-194-3P can reduce the resistance induced by LINC00663. ② Arteannuin B, a compound obtained from famous Chinese material medica “Artemisia annua L.” could improve the chemotherapy sensitivity of NSCLC cells by inhibiting the expression of LINC00663. Therefore, we propose that arteannuin B can regulate the complementary "adsorption" function of mir-194-3p by LINC00663 to attenuate the post-transcriptional inhibitory effect of target genes and activate down-stream related signaling pathways, thereby reducing the chemotherapy-resistance of NSCLC cells. This project intends to confirm the regulatory network and molecular mechanism of arteannuin B, LINC00663, mir-194-3p and down-stream target genes for chemotherapy resistance of NSCLC through systematically studies, and offer new ideas and scientific basis for the role of compounds from Chinese materia medica plays as antitumor drug in preventing and treating advanced NSCLC chemotherapy drug resistance.