Waltonitone
目录号 : GC26046Waltonitone, an ursane-type pentacyclic triterpene extracted from Gentiana waltonii Burkill, exerts anti-tumor effect.
Cas No.:1252676-55-3
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Waltonitone, an ursane-type pentacyclic triterpene extracted from Gentiana waltonii Burkill, exerts anti-tumor effect.
| Cas No. | 1252676-55-3 | SDF | Download SDF |
| 分子式 | C30H48O2 | 分子量 | 440.7 |
| 溶解度 | DMSO: 15 mg/mL (34.04 mM);; | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.2691 mL | 11.3456 mL | 22.6912 mL |
| 5 mM | 0.4538 mL | 2.2691 mL | 4.5382 mL |
| 10 mM | 0.2269 mL | 1.1346 mL | 2.2691 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Waltonitone induces apoptosis through mir-663-induced Bcl-2 downregulation in non-small cell lung cancer
Tumour Biol 2015 Feb;36(2):871-6.PMID:25301444DOI:10.1007/s13277-014-2704-4.
Our previous study reported that Waltonitone treatment inhibited proliferation and induced apoptosis of lung cancer cells. However, the mechanism of waltonitone-induced toxicity remains unclear. In the present study, we treated H460 and H3255 lung cancer cells using different concentration of Waltonitone (0, 10, 20, 30 μmol/L). We observed that Waltonitone inhibited cell viability and induced apoptosis in a concentration dependent manner, with upregulation of caspase-3 cleavage. We also observed upregulation of miR-663, a potential tumor suppressor, after Waltonitone treatment. Suppression of miR-663 function using miR-663 inhibitor partly alleviated cell toxicity induced by Waltonitone. In addition, both Waltonitone treatment and transfection of miR-663 mimic upregulated Bcl-2 mRNA and protein expression. Bcl-2 transfection alleviated waltonitone-induced toxicity. Furthermore, transfection of miR-663 inhibitor upregulated Bcl-2 levels in both cell lines. In summary, the present study demonstrated that Waltonitone induced apoptosis of lung cancer cells through, at least partly, miR-663-induced Bcl-2 downregulation.
Waltonitone induces human hepatocellular carcinoma cells apoptosis in vitro and in vivo
Cancer Lett 2009 Dec 28;286(2):223-31.PMID:19539424DOI:10.1016/j.canlet.2009.05.023.
Waltonitone, a new ursane-type pentacyclic triterpene isolated from Gentian waltonii Burkill significantly inhibited human hepatocellular carcinoma BEL-7402 cells growth. Apoptosis induced by Waltonitone was characterized by AO/EB staining and flow cytometric analysis. Apoptosis microarray assay results showed BCL-2 family genes might especially play an important role in waltonitone-induced apoptosis. RT-PCR and Western blotting analysis showed that Waltonitone could induce tumor cell apoptosis via both death receptor and mitochondria pathways. Meanwhile, the inhibitory effect of Waltonitone was examined in vivo using BEL-7402 tumor cells xenografted into athymic mice model. In summary, these studies demonstrated that Waltonitone might inhibit hepatocellular carcinoma cells growth and induce apoptosis in vitro and in vivo.
Waltonitone inhibits proliferation of hepatoma cells and tumorigenesis via FXR-miR-22-CCNA2 signaling pathway
Oncotarget 2016 Nov 15;7(46):75165-75175.PMID:27738335DOI:10.18632/oncotarget.12614.
Waltonitone (WA), an ursane-type pentacyclic triterpene extracted from Gentiana waltonii Burkill, was recently appeared to exert anti-tumor effect. However, the biological underpinnings underlying the role of WA in hepatocellular carcinoma (HCC) cells have not been completely elucidated. Our previous report indicated that the FXR-regulated miR-22-CCNA2 pathway contributed to the progression and development of HCC. Besides, a wide spectrum of microRNAs (miRNAs) could be up- or down-regulated upon WA treatment, including miR-22. Hence, we aimed to determine whether WA inhibited HCC cell proliferation via the FXR-miR-22-CCNA2 axis. In this study, we observed a significant downregulation of FXR and miR-22, along with upregulation of CCNA2 in 80 paired tumors relative to adjacent normal tissues of HCC subjects, which were obtained from the available GEO database in NCBI (GSE22058). Furthermore, we validated the expression patterns of these three targets in another set of HCC samples and found the highly correlation within each other. Additionally, our data demonstrated that WA induced miR-22 and repressed CCNA2 in HCC cells, which contributed to the cell proliferation arrest. In addition, evidence suggested that either miR-22 silencing or FXR knockdown reversed the diminished CCNA2 expression as well as cell proliferation inhibition caused by WA treatment and WA inhibited tumor masses in vivo in a subcutaneous xenograft mouse model of HCC. Overall, our data indicated that WA inhibited HCC cell proliferation and tumorigenesis through miR-22-regulated CCNA2 repression, which was at least partially through FXR modulation.
Suppression of growth of A549 lung cancer cells by Waltonitone and its mechanisms of action
Oncol Rep 2012 Sep;28(3):1029-35.PMID:22710478DOI:10.3892/or.2012.1869.
Natural compounds are a great source of cancer chemotherapeutic agents. Our investigation indicates that Waltonitone, a triterpene extracted from medicinal plants, inhibits the proliferation of A549 cells in a concentration- and time-dependent manner. Waltonitone induced apoptosis of A549 cells in a concentration-dependent manner, as determined by fluorescence microscopy and flow cytometry. The apoptosis was accompanied by increased Bax protein levels and decreased Bcl-2 protein levels in A549 cells. Furthermore, the treatment of A549 cells with Waltonitone altered the expression of miRNAs. We found that 27 miRNAs were differentially expressed in waltonitone-treated cells, of which 8 miRNAs target genes related to cell proliferation and apoptosis. In summary, our results demonstrate that Waltonitone has a significant inhibitory effect on the proliferation of A549 cells. It is possible that upregulation of Bax/Bcl-2 and regulation of expression of specific miRNAs play a role in inhibition of proliferation and induction of apoptosis in waltonitone-treated cells. Waltonitone can be applied to lung carcinoma as a chemotherapeutic candidate.
[WT inhibit human hepatocellular carcinoma BEL-7402 cells growth by modulating Akt and ERK1/2 phosphorylation]
Zhongguo Zhong Yao Za Zhi 2009 Dec;34(24):3277-80.PMID:20353018doi
Objective: To investigate effects of Akt and ERK1/2 signaling pathways on Waltonitone (WT) induced cell growth inhibition in human hepatocellular carcinoma BEL-7402 cells. Method: Cell viability of BEL-7402 cells was examined using MTT assay. Phosphorylation of E Akt and RK1/2 were detected by Western blot analysis, while cell cycle distribution of BEL7402 cells was analyzed by flow cytometry. Result: WT could inhibit the BEL-7402 cells growth, induce the S-phase cell cycle arrest, activate Akt and ERK1/2 phosporylation. Moreover, the cell growth inhibition and S-phase cell cycle arrest induction of WT on BEL-7402 cells could be blocked by Akt and ERK1/2 inhibitors. Conclusion: WT induce the cell cycle arrest and inhibit the cell growth on BEL-7402 cells by modulating Akt and ERK1/2 phosphorylation.