Britannin suppresses MCF-7 breast cancer cell growth by inducing apoptosis and inhibiting autophagy.

IF 1.9 Q3 CHEMISTRY, MEDICINAL Avicenna Journal of Phytomedicine Pub Date : 2024-01-01 DOI:10.22038/AJP.2023.22995
Sadegh Rajabi, Mahboubeh Irani, Marzieh Moeinifard, Maryam Hamzeloo-Moghadam
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Abstract

Objective: 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.

Materials and methods: 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.

Results: 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.

Conclusion: 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.

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布列塔尼通过诱导细胞凋亡和抑制自噬来抑制 MCF-7 乳腺癌细胞的生长。
目的:乳腺癌是妇女死于癌症的主要原因。布列塔尼是一种从茵陈中提取的倍半萜内酯化合物,具有抗肿瘤作用。我们旨在探讨布列塔尼对 MCF-7 乳腺癌细胞株凋亡和自噬的影响:采用 MTT 法检测刺五加对 MCF-7 细胞的细胞毒性影响。采用定量实时荧光定量PCR(qRT-PCR)技术对CASP3、BCL2、BCL2L1、STAT3、JAK2等凋亡相关基因和ATG1、ATG4、ATG5、ATG7、ATG12、BECN1、MAP1LC3A等自噬标志物的表达水平进行定量。采用 Western 印迹法评估 caspase 3、磷酸化 JAK2、磷酸化 STAT3、ATG1、ATG4、ATG5、Beclin1 和 LC-III 的含量:结果:与对照组相比,用不同浓度的溴丹宁处理 MCF-7 细胞会显著降低这些细胞的活力。这种化合物能明显提高促凋亡的caspase-3的表达,但不影响抗凋亡的BCL2和BCL2L1的水平。布列塔尼宁能降低磷酸化形式的 JAK2 和 STAT3 蛋白水平,从而阻断 JAK/STAT 通路。布列塔尼对MCF-7细胞的影响导致ATG4、ATG5、Beclin1和LCIII等四种自噬因子表达量减少:布列塔尼通过阻断JAK/STAT通路的机制诱导MCF-7细胞凋亡。此外,布列塔尼还能抑制这些癌细胞的自噬。这表明布列塔尼可作为抑制乳腺肿瘤的药物或增强抗乳腺癌药物效果的辅助药物。
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来源期刊
Avicenna Journal of Phytomedicine
Avicenna Journal of Phytomedicine CHEMISTRY, MEDICINAL-
CiteScore
3.40
自引率
4.50%
发文量
17
审稿时长
6 weeks
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