P2X7 promotes metastatic spreading and triggers release of miRNA-containing exosomes and microvesicles from melanoma cells

作者
Anna Pegoraro,Elena De Marchi,Manuela Ferracin,Elisa Orioli,Michele Zanoni,Cristian Bassi,Anna Tesei,Marina Capece,Emi Dika,Massimo Negrini,Francesco Di Virgilio,Elena Adinolfi
出处
期刊:Cell Death and Disease [Springer Nature]
卷期号:12 (12): 1088-1088 被引量:102
标识
DOI:10.1038/s41419-021-04378-0
摘要

Tumor growth and metastatic spreading are heavily affected by the P2X7 receptor as well as microvesicles and exosomes release into the tumor microenvironment. P2X7 receptor stimulation is known to trigger vesicular release from immune and central nervous system cells. However, P2X7 role in microvesicles and exosomes delivery from tumor cells was never analyzed in depth. Here we show that P2X7 is overexpressed in patients affected by metastatic malignant melanoma and that its expression closely correlates with reduced overall survival. Antagonism of melanoma cell-expressed P2X7 receptor inhibited in vitro anchorage-independent growth and migration and in vivo dissemination and lung metastasis formation. P2X7 stimulation triggered the release of miRNA-containing microvesicles and exosomes from melanoma cells, profoundly altering the nature of their miRNA content, as well as their dimensions and quantity. Among the more than 200 miRNAs that we found up-or-down-modulated for each vesicular fraction tested, we identified three miRNAs, miR-495-3p, miR-376c-3p, and miR-6730-3p, that were enriched in both the exosome and microvesicle fraction in a P2X7-dependent fashion. Interestingly, upon transfection, these miRNAs promoted melanoma cell growth or migration, and their vesicular release was minimized by P2X7 antagonism. Our data unveil an exosome/microvesicle and miRNA-dependent mechanism for the pro-metastatic activity of the P2X7 receptor and highlight this receptor as a suitable prognostic biomarker and therapeutic target in malignant melanoma.

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
木木完成签到 ,获得积分10
刚刚
zz完成签到,获得积分10
刚刚
芝士奶盖完成签到 ,获得积分10
1秒前
科研通AI6.4应助liuyue采纳,获得10
1秒前
酷酷宛完成签到,获得积分10
1秒前
imoon发布了新的文献求助10
2秒前
飞天817完成签到,获得积分10
2秒前
3秒前
高大的向南完成签到,获得积分10
3秒前
今后应助小懒采纳,获得10
4秒前
4秒前
多情方盒完成签到,获得积分10
4秒前
啦啦啦完成签到,获得积分10
4秒前
5秒前
雪碧和果冻完成签到,获得积分10
5秒前
难过的又柔完成签到,获得积分10
6秒前
一口一个柚子完成签到 ,获得积分10
6秒前
苗条的晓夏完成签到,获得积分10
7秒前
zinechoo完成签到,获得积分10
7秒前
Fang完成签到 ,获得积分10
7秒前
吃吃吃完成签到,获得积分10
8秒前
zx完成签到,获得积分10
8秒前
现实的宝马完成签到,获得积分10
8秒前
WizBLue完成签到,获得积分10
9秒前
AbOO完成签到,获得积分10
9秒前
9秒前
甜美的盼晴完成签到 ,获得积分10
9秒前
杀出个黎明举报szyyyyy求助涉嫌违规
11秒前
稀罕你完成签到,获得积分10
11秒前
宅在图书馆2完成签到,获得积分10
11秒前
12秒前
PSQ完成签到 ,获得积分10
13秒前
又晴完成签到,获得积分20
13秒前
林大侠完成签到,获得积分10
14秒前
领导范儿应助zsk采纳,获得10
14秒前
机智的寻琴完成签到,获得积分10
14秒前
洁净的酬海完成签到 ,获得积分10
14秒前
077完成签到,获得积分10
15秒前
绿豆粉腻子膏完成签到,获得积分10
15秒前
15秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Rosenblum, Global Change Biology 800
自動車の空力技術 800
Essentials of Carbohydrate Chemistry and Biochemistry, 4th Edition 800
Organizational Behavior 510
Management and the Arts 510
Matrix Methods in Data Mining and Pattern Recognition Second Edition 510
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 计算机科学 化学工程 工程类 有机化学 物理 复合材料 生物化学 内科学 细胞生物学 基因 遗传学 免疫学 冶金 光电子学 癌症研究
热门帖子
关注 科研通微信公众号,转发送积分 7778662
求助须知:如何正确求助?哪些是违规求助? 9318949
关于积分的说明 20367643
捐赠科研通 7365761
什么是DOI,文献DOI怎么找? 3319232
关于科研通互助平台的介绍 2467276
邀请新用户注册赠送积分活动 2334719