Folic Acid-Modified Liposome Quercetin Induces Apoptosis of Triple-Negative Breast Cancer Cells via Mitochondrial Apoptosis Mediated by JAK2/STAT3 Signaling Pathway
10.3971/j.issn.1000-8578.2024.23.1390
- VernacularTitle:叶酸修饰脂质体槲皮素经JAK2/STAT3信号通路介导的线粒体凋亡途径诱导三阴性乳腺癌细胞凋亡
- Author:
Fengxia CHEN
1
,
2
,
3
;
Feifei PU
Author Information
1. 430071 武汉,武汉大学中南医院肿瘤放化疗科
2. 430071 武汉,湖北省肿瘤医学临床研究中心
3. 430071 武汉,肿瘤生物学行为湖北省重点实验室
- Keywords:
Triple-negative breast cancer;
Folic acid-modified liposome quercetin;
Mitochondrial apoptosis pathway;
JAK2/STAT3 signaling pathway
- From:
Cancer Research on Prevention and Treatment
2024;51(7):554-560
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of folic acid-modified liposome quercetin(FLQ)on the proliferation and apoptosis of triple negative breast cancer(TNBC)cells and explore its underlying mech-anism.Methods CCK-8 was used to detect the effect of FLQ on TNBC cell viability.Colony formation assay was conducted to detect the effect of FLQ on TNBC cell proliferation.Flow cytometry was performed to detect the effect of FLQ on TNBC cell apoptosis,the levels of intracellular ROS,and mitochondrial membrane potential.Western blot analysis was conducted to detect the expression levels of JAK2/STAT3 signaling pathway-related and apoptosis-related proteins.Results FLQ inhibited the proliferation and promoted the apoptosis of MDA-MB-231 cells(P=0.023,P<0.001).It promoted mitochondrial membrane potential collapse and increased the intracellular ROS levels of MDA-MB-231 cells(P=0.003,P=0.034);inhibited the phosphorylation levels of JAK2 and STAT3;upregulated the expression levels of the proapo-ptotic proteins Bax,Bak,cytochrome C,and Cleaved-Caspase-3(P<0.001,P<0.001);and downregulated the expression levels of the antiapoptotic proteins Bcl2 and Bcl-xL(P=0.037,0.028).Conclusion FLQ inhibits the proliferation and induces the apoptosis of MDA-MB-231 cells.These effects may be related to the activa-tion of the mitochondrial apoptosis pathway through the inhibition of the JAK2/STAT3 signaling pathway.
