Rutaecarpine enhances the anti-diabetic activity and hepatic distribution of metformin via up-regulation of Oct1 in diabetic rats

Song, Xian-Mei; Li, Bingjie; Zhang, Yanyan; Ge, Wenjing; Zhang, She-Feng; Wei-feng, Cui; Geng-sheng, LI; Liang, Ruifeng

doi:10.1080/00498254.2021.1926573

Cited by 1 publication

(1 citation statement)

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“…And the signaling pathway can also be further investigated and verified in the miR-149-3p/S100A4-mediated BC process. According to literature reports (26,31,(48)(49)(50), the research of RUT on various diseases (heart disease, ulcerative colitis, obesity, tumors) is still based on cell and animal models, and its therapeutic dose and effect on patients in clinical practice also need to be further explored.…”

Section: Discussionmentioning

confidence: 99%

Rutaecarpine prevents the malignant biological properties of breast cancer cells by the miR-149-3p/S100A4 axis

Xiong¹,

Xiong²,

Shan³

2022

Ann Transl Med

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Background Breast cancer (BC) is a frequent malignancy that endangers women’s health, and its fatality rate ranks 1st among female malignancies. Research has shown that rutaecarpine (RUT), which is a Chinese herbal medicine, blocks the proliferation of cancer cells by a variety of molecular mechanisms. However, the possible effects and mechanism of RUT in the autophagy and angiogenesis of BC cells has not been clearly articulated. Methods MiR-149-3p and S100A4 expression levels were assessed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and the optimal concentration and time of RUT was confirmed by Cell Counting Kit-8 (CCK-8) assays of the BC cells. After treatment, changes in cell proliferation and the cell cycle were evaluated by CCK-8 assays, clone formation assays, and flow cytometry, and the levels of apoptosis, autophagy, and angiogenesis-related proteins were identified by Western blot. The targeted regulation of miR-149-3p on S100A4 was also examined by luciferase reporter assays. Results We found that RUT inhibited cell growth and upregulated miR-149-3p in MDA-MB-231 cells. In relation to the biological function activity, RUT attenuated proliferation and angiogenesis, and induced cell-cycle arrest and autophagy by miR-149-3p in the MDA-MB-231 cells. Additionally, miR-149-3p downregulated S100A4 by targeting binding to S100A4, and S100A4 was required for miR-149-3p to play a role in BC progression. We also discovered that an autophagy agonist (rapamycin) or an angiogenesis inhibitor (TNP-470) changed BC progression mediated by the RUT/miR-149-3p/S100A4 axis. Conclusions RUT blocks the malignant behaviors of BC cells through the miR-149-3p/S100A4 axis and thus alters autophagy and angiogenesis. Thus, the RUT-mediated miR-149-3p/S100A4 axis might be an underlying therapeutic agent and target for BC.

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