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灯盏乙素通过内质网-线粒体轴钙内流促进细胞死亡并抑制上皮性卵巢癌中的丝氨酸蛋白酶抑制剂B11（SERPINB11）

Eupatilin Promotes Cell Death by Calcium Influx through ER-Mitochondria Axis with SERPINB11 Inhibition in Epithelial Ovarian Cancer.

作者信息

Lee Jin-Young, Bae Hyocheol, Yang Changwon, Park Sunwoo, Youn Byung-Soo, Kim Han-Soo, Song Gwonhwa, Lim Whasun

机构信息

Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.

Department of Biotechnology, Institute of Animal Molecular Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul 02841, Korea.

出版信息

Cancers (Basel). 2020 Jun 3;12(6):1459. doi: 10.3390/cancers12061459.

DOI:10.3390/cancers12061459
PMID:32503295
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7353024/
Abstract

Ovarian cancer is the leading cause of gynecological cancer-related mortality. The anticancer effect of eupatilin, a family of flavonoids, is known in many cancer types, but it is unclear what mechanism it plays in ovarian cancer. In this study, eupatilin promoted cell death of ovarian cancer cells by activating caspases, cell cycle arrest, reactive oxygen species (ROS) generation, calcium influx, disruption of the endoplasmic reticulum (ER)-mitochondria axis with SERPINB11 inhibition, and downregulation of phosphoinositide 3-kinase (PI3K) and mitogen activated protein kinase (MAPK) pathways. Additionally, eupatilin-reduced SERPINB11 expression enhanced the effect of conventional chemotherapeutic agents against ovarian cancer cell progression. Cotreatment with siSERPINB11 and eupatilin increased calcium-ion-dependent apoptotic activity in ovarian cancer cells. Although there were no significant toxic effects of eupatilin on embryos, eupatilin completely inhibited tumorigenesis in a zebrafish xenograft model. In addition, eupatilin suppressed angiogenesis in zebrafish transgenic models. Collectively, downregulating SERPINB11 with eupatilin against cancer progression may improve therapeutic activity.

摘要

卵巢癌是妇科癌症相关死亡的主要原因。黄酮类化合物之一的灯盏花乙素在多种癌症类型中具有抗癌作用，但尚不清楚其在卵巢癌中发挥何种机制。在本研究中，灯盏花乙素通过激活半胱天冬酶、诱导细胞周期停滞、产生活性氧（ROS）、引起钙内流、抑制丝氨酸蛋白酶抑制剂B11（SERPINB11）从而破坏内质网（ER）-线粒体轴，以及下调磷脂酰肌醇3激酶（PI3K）和丝裂原活化蛋白激酶（MAPK）信号通路，促进卵巢癌细胞死亡。此外，灯盏花乙素降低SERPINB11的表达增强了传统化疗药物对卵巢癌细胞进展的抑制作用。siSERPINB11与灯盏花乙素联合处理增加了卵巢癌细胞中钙离子依赖性凋亡活性。虽然灯盏花乙素对胚胎没有明显的毒性作用，但在斑马鱼异种移植模型中，灯盏花乙素完全抑制了肿瘤发生。此外，灯盏花乙素在斑马鱼转基因模型中抑制了血管生成。总之，用灯盏花乙素下调SERPINB11以对抗癌症进展可能会提高治疗活性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8bf/7353024/570aa8bd2577/cancers-12-01459-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8bf/7353024/cebdf4adfb2c/cancers-12-01459-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8bf/7353024/baa8d661d0fe/cancers-12-01459-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8bf/7353024/e6e1a0267904/cancers-12-01459-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8bf/7353024/f421f7ab8bf9/cancers-12-01459-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8bf/7353024/2f2826958816/cancers-12-01459-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8bf/7353024/327f3c86b7dc/cancers-12-01459-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8bf/7353024/7f200fbeecce/cancers-12-01459-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8bf/7353024/570aa8bd2577/cancers-12-01459-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8bf/7353024/cebdf4adfb2c/cancers-12-01459-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8bf/7353024/baa8d661d0fe/cancers-12-01459-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8bf/7353024/e6e1a0267904/cancers-12-01459-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8bf/7353024/f421f7ab8bf9/cancers-12-01459-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8bf/7353024/2f2826958816/cancers-12-01459-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8bf/7353024/327f3c86b7dc/cancers-12-01459-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8bf/7353024/7f200fbeecce/cancers-12-01459-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8bf/7353024/570aa8bd2577/cancers-12-01459-g008.jpg

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