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Arnicolide C Suppresses Tumor Progression by Targeting 14-3-3θ in Breast Cancer

文献类型：期刊论文

作者Liu, Zhengrui6; Lyu, Xiaodan6; Chen, Jiaxu5; Zhang, Benteng6; Xie, Siman6; Yuan, Yan4; Sun, Li6; Yuan, Shengtao3; Yu, Hong2; Ding, Jian1,3
刊名PHARMACEUTICALS
出版日期2024-02-01
卷号17期号:2页码:14
关键词arnicolide C breast neoplasms cell proliferation 14-3-3 theta PDX
DOI10.3390/ph17020224
通讯作者Ding, Jian(jding@simm.ac.cn) ; Yang, Mei(yangmei@cpu.edu.cn)
英文摘要Background: Arnicolide C, which is isolated from Centipeda minima, has excellent antitumor effects. However, the potential impacts and related mechanisms of action of arnicolide C in breast cancer remain unknown. Methods: The viability of breast cancer cells was measured using MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and colony formation assays. For analysis of apoptosis and the cell cycle, flow cytometry was used. A molecular docking approach was used to explore the possible targets of arnicolide C. Western blot analysis was used to detect changes in the expression of 14-3-3 theta and proteins in related pathways after arnicolide C treatment in breast cancer cells. The anti-breast cancer effect of arnicolide C in vivo was evaluated by establishing cell-derived xenograft (CDX) and patient-derived xenograft (PDX) models. Results: Arnicolide C inhibited proliferation, increased apoptosis, and induced G1 arrest. In particular, molecular docking analysis indicated that arnicolide C binds to 14-3-3 theta. Arnicolide C reduced 14-3-3 theta expression and inhibited its downstream signaling pathways linked to cell proliferation. Similar results were obtained in the CDX and PDX models. Conclusion: Arnicolide C can have an anti-breast cancer effect both in vitro and in vivo and can induce cell cycle arrest and increase apoptosis in vitro. The molecular mechanism may be related to the effect of arnicolide C on the expression level of 14-3-3 theta. However, the specific mechanism through which arnicolide C affects 14-3-3 theta protein expression still needs to be determined.
WOS关键词STRUCTURAL BASIS ; DOWN-REGULATION ; PROTEIN ; PROLIFERATION ; APOPTOSIS ; OVEREXPRESSION ; 14-3-3-GAMMA ; METASTASIS ; CELLS
资助项目National Natural Science Foundation of China
WOS研究方向Pharmacology & Pharmacy
语种英语
WOS记录号WOS:001172016100001
出版者MDPI
源URL[http://119.78.100.183/handle/2S10ELR8/312526]  
专题新药研究国家重点实验室
通讯作者Ding, Jian; Yang, Mei
作者单位1.Chinese Acad Sci, Shanghai Inst Mat Med, State Key Lab Drug Res, Shanghai 201203, Peoples R China
2.Nanjing Med Univ, Affiliated Taizhou Peoples Hosp, Dept Pathol, Taizhou 225300, Peoples R China
3.China Pharmaceut Univ, Jiangsu Ctr Pharmacodynam Res & Evaluat, Nanjing 210009, Peoples R China
4.China Pharmaceut Univ, Sch Pharm, Dept Pharmacol, Nanjing 210009, Peoples R China
5.Lanzhou Univ, Coll Pharm, Lanzhou 730000, Peoples R China
6.China Pharmaceut Univ, Jiangsu Key Lab Drug Screening, Nanjing 210009, Peoples R China
推荐引用方式
GB/T 7714		 Liu, Zhengrui,Lyu, Xiaodan,Chen, Jiaxu,et al. Arnicolide C Suppresses Tumor Progression by Targeting 14-3-3θ in Breast Cancer[J]. PHARMACEUTICALS,2024,17(2):14.
APA Liu, Zhengrui.,Lyu, Xiaodan.,Chen, Jiaxu.,Zhang, Benteng.,Xie, Siman.,...&Yang, Mei.(2024).Arnicolide C Suppresses Tumor Progression by Targeting 14-3-3θ in Breast Cancer.PHARMACEUTICALS,17(2),14.
MLA Liu, Zhengrui,et al."Arnicolide C Suppresses Tumor Progression by Targeting 14-3-3θ in Breast Cancer".PHARMACEUTICALS 17.2(2024):14.

入库方式： OAI收割

来源：上海药物研究所

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