乳腺癌是女性癌症相关死亡的主要原因。 Britannin 是一种从 Inula aucheriana 中提取的倍半萜内酯化合物，具有抗肿瘤特性。目的探讨不列颠宁对MCF-7乳腺癌细胞系凋亡和自噬的影响。采用MTT法评价不列颠宁对MCF-7细胞的细胞毒影响。使用定量实时 PCR (qRT) 对细胞凋亡相关基因（如 CASP3、BCL2、BCL2L1、STAT3 和 JAK2）的表达水平以及自噬标记物（包括 ATG1、ATG4、ATG5、ATG7、ATG12、BECN1 和 MAP1LC3A）的转录本进行定量。 -PCR）。采用Western blotting法检测caspase 3、磷酸化JAK2、磷酸化STAT3、ATG1、ATG4、ATG5、Beclin1和LC-III的含量。不同浓度的不列颠宁处理MCF-7细胞后，细胞活力明显受到抑制。与对照相比。该化合物显着升高促凋亡 caspase-3 的表达，但不影响抗凋亡 BCL2 和 BCL2L1 的水平。 Britannin 降低 JAK2 和 STAT3 蛋白磷酸化形式的水平，导致 JAK/STAT 通路阻断。 Britannin对MCF-7细胞的影响导致ATG4、ATG5、Beclin1和LCIII等四种自噬因子表达降低。Britannin通过阻断JAK/STAT的机制引发MCF-7细胞凋亡途径。此外，不列颠宁可以抑制这些癌细胞的自噬。这可能表明英国丹宁可以作为抑制乳腺肿瘤的药物或作为增强抗乳腺癌药物效果的佐剂。

Breast cancer is the main reason for cancer-related death in women. Britannin is a sesquiterpene lactone compound derived from Inula aucheriana with anti-tumor properties. We aimed to explore the impacts of britannin on apoptosis and autophagy in MCF-7 breast cancer cell line.The cytotoxic influences of britannin on MCF-7 cells were estimated by the MTT method. The expression levels of apoptosis-associated genes such as CASP3, BCL2, BCL2L1, STAT3, and JAK2 and transcripts of autophagy markers including ATG1, ATG4, ATG5, ATG7, ATG12, BECN1, and MAP1LC3A were quantified using quantitative real time-PCR (qRT-PCR). Western blotting method was used to evaluate the amount of caspase 3, phosphorylated JAK2, phosphorylated STAT3, ATG1, ATG4, ATG5, Beclin1, and LC-III.Treatment of MCF-7 cells with various concentrations of britannin remarkably hindered the viability of these cells compared to the controls. This compound significantly elevated the expression of pro-apoptotic caspase-3 but did not influence the levels of anti-apoptotic BCL2 and BCL2L1. Britannin decreased the levels of phosphorylated forms of JAK2 and STAT3 proteins causing the blockage of the JAK/STAT pathway. Four autophagy factors expressions, including ATG4, ATG5, Beclin1, and LCIII, were reduced due to the effect of britannin on MCF-7 cells.Britannin triggered apoptosis in MCF-7 cells by a mechanism that led to the blockade of the JAK/STAT pathway. Moreover, britannin prohibited autophagy in these cancer cells. This may suggest britannin as an agent for the suppression of breast tumors or as an adjutant for the enhancement of anti-breast cancer drugs effect.