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薏苡仁油通过破坏miR-205/S1PR1轴发挥抗三阴性乳腺癌作用。

Coix Seed Oil Exerts an Anti-Triple-Negative Breast Cancer Effect by Disrupting miR-205/S1PR1 Axis.

作者信息

Fang Ting, Jiang Yi-Xin, Chen Long, Huang Ling, Tian Xin-Hui, Zhou Yu-Dong, Nagle Dale G, Zhang Dan-Dan

机构信息

Interdisciplinary Integrative Medicine Research, Shanghai University of Traditional Chinese Medicine, Shanghai, China.

School of Pharmacy, Fujian University of Traditional Chinese Medicine, Fuzhou, China.

出版信息

Front Pharmacol. 2020 Sep 25;11:529962. doi: 10.3389/fphar.2020.529962. eCollection 2020.

DOI:10.3389/fphar.2020.529962
PMID:33101013
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7556270/
Abstract

Coix Seed Oil (CSO) possesses a wide range of pharmacological activities. Kanglaite Injection, a commercial product of CSO, has been used clinically as an anticancer drug in China for decades. However, its molecular mechanisms on triple-negative breast cancer (TNBC) remains to be elucidated. In this study, the effect of CSO was evaluated on murine TNBC 4T1 cells and the orthotopic tumor-bearing mouse model and underlying mechanisms were explored. CSO suppressed cell proliferation, colony formation , and tumor growth . miR-205-5p was substantially altered in CSO treated tumor tissues compared to the control group by miRNA-sequencing analysis. Sphingomyelin metabolism (SM) decreased in serum in model group compared to the control group, while it increased by CSO administration by lipid metabolomics analysis. The expression of sphingosine 1 phosphate receptor 1 (S1PR1), the critical effector of SM, was downregulated upon CSO treatment. Mechanically, miRNA-205 directly targeted S1PR1 to regulate SM and cell proliferation. CSO reduced the expression of S1PR1, cyclinD1, and phosphorylation levels of STAT3, MAPK, and AKT while upregulated p27. These results revealed that CSO exerted an anti-TNBC effect the miR-205/S1PR1 axis to regulate sphingomyelin metabolism, and the downstream STAT3/MAPK/AKT signal pathways were partly involved.

摘要

薏苡仁油（CSO）具有广泛的药理活性。康莱特注射液是CSO的一种商业产品，在中国已作为抗癌药物临床使用数十年。然而，其对三阴性乳腺癌（TNBC）的分子机制仍有待阐明。在本研究中，评估了CSO对小鼠TNBC 4T1细胞和原位荷瘤小鼠模型的作用，并探讨了其潜在机制。CSO抑制细胞增殖、集落形成和肿瘤生长。通过miRNA测序分析，与对照组相比，CSO处理的肿瘤组织中miR-205-5p发生了显著变化。脂质代谢组学分析显示，与对照组相比，模型组血清中鞘磷脂代谢（SM）降低，而CSO给药后其增加。CSO处理后，鞘磷脂代谢的关键效应分子鞘氨醇-1-磷酸受体1（S1PR1）的表达下调。机制上，miRNA-205直接靶向S1PR1以调节SM和细胞增殖。CSO降低了S1PR1、细胞周期蛋白D1的表达以及STAT3、MAPK和AKT的磷酸化水平，同时上调了p27。这些结果表明，CSO通过miR-205/S1PR1轴发挥抗TNBC作用，调节鞘磷脂代谢，且下游STAT3/MAPK/AKT信号通路部分参与其中。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2162/7556270/9c7d101c7890/fphar-11-529962-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2162/7556270/920a21748c8e/fphar-11-529962-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2162/7556270/26121e775f8e/fphar-11-529962-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2162/7556270/ee0b7a9da825/fphar-11-529962-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2162/7556270/87e9a46fcf60/fphar-11-529962-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2162/7556270/c818c177c7aa/fphar-11-529962-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2162/7556270/9c7d101c7890/fphar-11-529962-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2162/7556270/920a21748c8e/fphar-11-529962-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2162/7556270/26121e775f8e/fphar-11-529962-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2162/7556270/ee0b7a9da825/fphar-11-529962-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2162/7556270/87e9a46fcf60/fphar-11-529962-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2162/7556270/c818c177c7aa/fphar-11-529962-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2162/7556270/9c7d101c7890/fphar-11-529962-g006.jpg

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