Lycorine inhibits pancreatic cancer cell growth and neovascularization by inducing Notch1 degradation and downregulating key vasculogenic genes

石蒜碱 胰腺癌 癌症研究 血管生成 细胞生长 癌症 生物 药理学 医学 内科学 生物碱 生物化学 植物
作者
Jindan Qi,Mei Meng,Juntao Liu,Xiaoxiao Song,Yu Chen,Yuxi Liu,Xu Li,Zhou Zhou,Xiang Huang,Xiaohua Wang,Quansheng Zhou,Zhe Zhao
出处
期刊:Biochemical Pharmacology [Elsevier BV]
卷期号:217: 115833-115833 被引量:10
标识
DOI:10.1016/j.bcp.2023.115833
摘要

Pancreatic cancer is highly metastatic and lethal with an increasing incidence globally and a 5-year survival rate of only 8%. One of the factors contributing to the high mortality is the lack of effective drugs in the clinical setting. We speculated that effective compounds against pancreatic cancer exist in natural herbs and explored active small molecules among traditional Chinese medicinal herbs. The small molecule lycorine (MW: 323.77) derived from the herb Lycoris radiata inhibited pancreatic cancer cell growth with an IC50 value of 1 μM in a concentration-dependent manner. Lycorine markedly reduced pancreatic cancer cell viability, migration, invasion, neovascularization, and gemcitabine resistance. Additionally, lycorine effectively suppressed tumor growth in mouse xenograft models without obvious toxicity. Pharmacological studies revealed that the levels and half-life of Notch1 oncoprotein in the pancreatic cancer cells Panc-1 and Patu8988 were notably reduced. Moreover, the expression of the key vasculogenic genes Semaphorin 4D (Sema4D) and angiopoietin-2 (Ang-2) were also significantly inhibited by lycorine. Mechanistically, lycorine strongly triggered the degradation of Notch1 oncoprotein through the ubiquitin–proteasome system. In conclusion, lycorine effectively inhibits pancreatic cancer cell growth, migration, invasion, neovascularization, and gemcitabine resistance by inducing degradation of Notch1 oncoprotein and downregulating the key vasculogenic genes Sema4D and Ang-2. Our findings provide a new therapeutic candidate and treatment strategy against pancreatic cancer.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
小研完成签到,获得积分10
1秒前
辛勤曼容完成签到 ,获得积分10
2秒前
初景发布了新的文献求助10
3秒前
踏雪寻梅关注了科研通微信公众号
3秒前
3秒前
倪大业666完成签到 ,获得积分10
4秒前
回忆的天空完成签到 ,获得积分10
4秒前
5秒前
傻傻的芷巧完成签到,获得积分10
6秒前
geo_xl完成签到 ,获得积分10
7秒前
8秒前
起点完成签到,获得积分10
9秒前
贝贝完成签到 ,获得积分10
9秒前
Ryu发布了新的文献求助10
9秒前
DW的应助被高昱菲采纳,获得10
10秒前
冷静新烟完成签到 ,获得积分10
12秒前
13秒前
牧青发布了新的文献求助10
13秒前
mawen完成签到 ,获得积分10
13秒前
14秒前
fan完成签到 ,获得积分10
14秒前
14秒前
毛小毛发布了新的文献求助10
14秒前
秋风的应助被冬虫夏草采纳,获得10
14秒前
小学僧发布了新的文献求助10
16秒前
17秒前
一二完成签到,获得积分10
18秒前
ljl发布了新的文献求助10
18秒前
喜悦蚂蚁完成签到,获得积分10
18秒前
19秒前
20秒前
21秒前
22秒前
22秒前
小熊发布了新的文献求助10
23秒前
初景发布了新的文献求助10
23秒前
yx发布了新的文献求助10
24秒前
打打的应助被后笑晴采纳,获得10
25秒前
26秒前
笨笨发布了新的文献求助10
26秒前
高分求助中
(应助此贴封号)通过应助OA文献获取积分 10000
Rosenblum, Global Change Biology 800
Computational Chemical Reaction Engineering: Modeling, Simulation, and Design with MATLAB 600
Organizational Behavior 510
Management and the Arts 510
A Will for the Machine: Computerization, Automation, and the Arts in South Africa 400
Decentring Leadership 400
热门求助领域 (近24小时)
化学 材料科学 医学 生物 计算机科学 工程类 纳米技术 内科学 物理 有机化学 化学工程 生物化学 复合材料 光电子学 细胞生物学 心理学 量子力学 催化作用 物理化学 电极
热门帖子
关注 科研通微信公众号,转发送积分 7810327
求助须知:如何正确求助?哪些是违规求助? 9342131
关于积分的说明 20510929
捐赠科研通 7403143
什么是DOI,文献DOI怎么找? 3329356
关于科研通互助平台的介绍 2476243
邀请新用户注册赠送积分活动 2348249