PDF(Pubmed)
Abstract：
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.
摘要：
■乳腺癌是女性癌症相关死亡的主要原因。Britannin是衍生自Inulaaucheriana的倍半萜内酯化合物，具有抗肿瘤特性。本研究旨在探讨Britannin对乳腺癌MCF-7细胞凋亡和自噬的影响。
■通过MTT方法评估了Britannin对MCF-7细胞的细胞毒性影响。使用定量实时PCR(qRT-PCR)对细胞凋亡相关基因(如CASP3、BCL2、BCL2L1、STAT3和JAK2)和自噬标志物(包括ATG1、ATG4、ATG5、ATG7、ATG12、BECN1和MAP1LC3A)的转录物的表达水平进行定量。Western印迹法用于评估caspase3，磷酸化JAK2，磷酸化STAT3，ATG1，ATG4，ATG5，Beclin1和LC-III的量。
■与对照相比,用各种浓度的Britannin处理MCF-7细胞显著阻碍了这些细胞的活力。该化合物显著提高促凋亡半胱天冬酶-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途径的阻断。四种自噬因子的表达，包括ATG4、ATG5、Beclin1和LCIII，由于Britannin对MCF-7细胞的作用而减少。
■Britannin通过导致JAK/STAT通路阻断的机制触发MCF-7细胞的凋亡。此外，Britannin禁止这些癌细胞中的自噬。这可能表明Britannin可作为抑制乳腺肿瘤的药物或作为增强抗乳腺癌药物作用的辅助剂。
■通过MTT方法评估了Britannin对MCF-7细胞的细胞毒性影响。使用定量实时PCR(qRT-PCR)对细胞凋亡相关基因(如CASP3、BCL2、BCL2L1、STAT3和JAK2)和自噬标志物(包括ATG1、ATG4、ATG5、ATG7、ATG12、BECN1和MAP1LC3A)的转录物的表达水平进行定量。Western印迹法用于评估caspase3，磷酸化JAK2，磷酸化STAT3，ATG1，ATG4，ATG5，Beclin1和LC-III的量。
■与对照相比,用各种浓度的Britannin处理MCF-7细胞显著阻碍了这些细胞的活力。该化合物显著提高促凋亡半胱天冬酶-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途径的阻断。四种自噬因子的表达，包括ATG4、ATG5、Beclin1和LCIII，由于Britannin对MCF-7细胞的作用而减少。
■Britannin通过导致JAK/STAT通路阻断的机制触发MCF-7细胞的凋亡。此外，Britannin禁止这些癌细胞中的自噬。这可能表明Britannin可作为抑制乳腺肿瘤的药物或作为增强抗乳腺癌药物作用的辅助剂。
