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黄樟素B与阿霉素协同作用，通过活性氧介导的凋亡和自噬途径抑制胃癌细胞的增殖。

Flavokawain B and Doxorubicin Work Synergistically to Impede the Propagation of Gastric Cancer Cells via ROS-Mediated Apoptosis and Autophagy Pathways.

作者信息

Hseu You-Cheng, Lin Ruei-Wan, Shen Yi-Chun, Lin Kai-Yuan, Liao Jiunn-Wang, Thiyagarajan Varadharajan, Yang Hsin-Ling

机构信息

Department of Cosmeceutics, College of Pharmacy, China Medical University, Taichung 40402, Taiwan.

Department of Health and Nutrition Biotechnology, Asia University, Taichung 41354, Taiwan.

出版信息

Cancers (Basel). 2020 Sep 1;12(9):2475. doi: 10.3390/cancers12092475.

DOI:10.3390/cancers12092475
PMID:32882870
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7564097/
Abstract

Chalcone flavokawain B (FKB) possesses a chemopreventive and anti-cancer activity. Doxorubicin is a chemotherapeutic DNA intercalating agent widely used in malignancy treatment. The present study investigated whether synergistic effects exist between the combination of FKB (1.25-5 µg/mL) and doxorubicin (0.5 µg/mL) on the apoptosis and autophagy in human gastric cancer (AGS) cells, and the possible in vitro and in vivo mechanisms. The MTT assay measured cell viability. Various apoptotic-, autophagy-associated protein expression was determined by the Western blot technique. FKB+doxorubicin synergy was estimated by the Chou-Talalay combination index (CI) method. In vivo studies were performed on BALB/ mice. Results showed that compared to FKB/doxorubicin treatments, low doses of FKB+doxorubicin suppressed AGS cell growth. FKB potentiated doxorubicin-induced DNA fragmentation, apoptotic cell death, and enhanced doxorubicin-mediated mitochondrial, death receptor pathways. FKB+doxorubicin activated increased LC3-II accumulation, p62/SQSTM1 expression, and AVO formation as compared to the FKB/doxorubicin alone treatments indicating autophagy in these cells. The death mechanism in FKB+doxorubicin-treated AGS cells is due to the activation of autophagy. FKB+doxorubicin-mediated dysregulated Bax/Bcl-2, Beclin-1/Bcl-2 ratios suggested apoptosis, autophagy induction in AGS cells. FKB+doxorubicin-induced LC3-II/AVOs downregulation was suppressed due to an apoptotic inhibitor Z-VAD-FMK. Whereas, 3-methyladenine/chloroquine weakened FKB+doxorubicin-induced apoptosis (decreased DNA fragmentation/caspase-3). Activation of ERK/JNK may be involved in FKB+doxorubicin-induced apoptosis and autophagy. FKB+doxorubicin-triggered ROS generation, but NAC attenuated FKB+doxorubicin-induced autophagic (LC3 accumulation) and apoptotic (caspase-3 activation and PARP cleavage) cell death. FKB+doxorubicin blocked gastric cancer cell xenografts in nude mice in vivo as compared to FKB/doxorubicin alone treatments. FKB and doxorubicin wielded synergistic anti-tumor effects in gastric cancer cells and is a promising therapeutic approach.

摘要

查尔酮黄樟素B（FKB）具有化学预防和抗癌活性。阿霉素是一种化疗性DNA嵌入剂，广泛用于恶性肿瘤治疗。本研究调查了FKB（1.25 - 5μg/mL）与阿霉素（0.5μg/mL）联合使用对人胃癌（AGS）细胞凋亡和自噬是否存在协同作用，以及可能的体外和体内机制。MTT法检测细胞活力。采用蛋白质免疫印迹技术测定各种凋亡相关蛋白和自噬相关蛋白的表达。通过Chou-Talalay联合指数（CI）法评估FKB +阿霉素的协同作用。在BALB/c小鼠上进行体内研究。结果表明，与FKB/阿霉素单独处理相比，低剂量的FKB +阿霉素抑制AGS细胞生长。FKB增强了阿霉素诱导的DNA片段化、凋亡细胞死亡，并增强了阿霉素介导的线粒体、死亡受体途径。与单独使用FKB/阿霉素处理相比，FKB +阿霉素激活增加了LC3-II积累、p62/SQSTM1表达和自噬空泡形成，表明这些细胞中存在自噬。FKB +阿霉素处理的AGS细胞中的死亡机制是由于自噬的激活。FKB +阿霉素介导的Bax/Bcl-2、Beclin-1/Bcl-2比值失调提示AGS细胞发生凋亡、自噬诱导。凋亡抑制剂Z-VAD-FMK抑制了FKB +阿霉素诱导的LC3-II/自噬空泡下调。而3-甲基腺嘌呤/氯喹减弱了FKB +阿霉素诱导的凋亡（DNA片段化/caspase-3减少）。ERK/JNK的激活可能参与FKB +阿霉素诱导的凋亡和自噬。FKB +阿霉素引发活性氧生成，但NAC减弱了FKB +阿霉素诱导的自噬（LC3积累）和凋亡（caspase-3激活和PARP裂解）细胞死亡。与单独使用FKB/阿霉素处理相比，FKB +阿霉素在体内阻断了裸鼠胃癌细胞异种移植。FKB和阿霉素在胃癌细胞中发挥协同抗肿瘤作用，是一种有前景的治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/7564097/01b0d90fd526/cancers-12-02475-g012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/7564097/0b8a391649ac/cancers-12-02475-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/7564097/8abbc94f744f/cancers-12-02475-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/7564097/7e92b77291b9/cancers-12-02475-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/7564097/48e9d6044734/cancers-12-02475-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/7564097/7bd8dab3bee0/cancers-12-02475-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/7564097/6c7ddf50538f/cancers-12-02475-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/7564097/a17f57f3c4dc/cancers-12-02475-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/7564097/877f88fbfab6/cancers-12-02475-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/7564097/c54a2c784f70/cancers-12-02475-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/7564097/91035e219f63/cancers-12-02475-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/7564097/5366eefc4d00/cancers-12-02475-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/7564097/01b0d90fd526/cancers-12-02475-g012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/7564097/0b8a391649ac/cancers-12-02475-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/7564097/8abbc94f744f/cancers-12-02475-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/7564097/7e92b77291b9/cancers-12-02475-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/7564097/48e9d6044734/cancers-12-02475-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/7564097/7bd8dab3bee0/cancers-12-02475-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/7564097/6c7ddf50538f/cancers-12-02475-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/7564097/a17f57f3c4dc/cancers-12-02475-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/7564097/877f88fbfab6/cancers-12-02475-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/7564097/c54a2c784f70/cancers-12-02475-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/7564097/91035e219f63/cancers-12-02475-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/7564097/5366eefc4d00/cancers-12-02475-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/7564097/01b0d90fd526/cancers-12-02475-g012.jpg

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