Cucurbitacin B CAS NO.6199-67-3

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General tips：For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
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Chemical Properties of Cucurbitacin B

Source of Cucurbitacin B

1 Bolbostemma sp. 2 Bryonia sp. 3 Cayaponia sp. 4 Chrysosplenium sp. 5 Citrullus sp. 6 Conobea sp. 7 Cucumis sp. 8 Cucurbita sp. 9 Ecballium sp. 10 Hemsleya sp. 11 Licania sp. 12 Luffa sp. 13 Melonis sp. 14 Morierina sp. 15 Trichosanthes sp. 16 Wilbrandia sp.

Biological Activity of Cucurbitacin B

Protocol of Cucurbitacin B

Preparing Stock Solutions of Cucurbitacin B

References on Cucurbitacin B

Cucurbitacin B inhibits proliferation and induces apoptosis via STAT3 pathway inhibition in A549 lung cancer cells.[Pubmed:25242136]

Mol Med Rep. 2014 Dec;10(6):2905-11.

Natural products are a great source of cancer chemotherapeutic agents. The present study was conducted to investigate whether Cucurbitacin B (CuB), one of the most potent and widely used cucurbitacins, inhibits proliferation and induces apoptosis in the A549 lung cancer cell line. Furthermore, CuB induced apoptosis of A549 cells in a -concentration-dependent manner, as determined by fluorescence microscopy, flow cytometry and transmission electron microscopy. The present study also demonstrated that CuB dose-dependently inhibited lung cancer cell proliferation, with cell cycle inhibition and cyclin B1 downregulation. Apoptosis induced by CuB was shown to be associated with cytochrome c release, B-cell lymphoma 2 downregulation and signal transducer and activator of transcription 3 pathway inhibition. CuB may prove to be a useful approach for the chemotherapy of lung cancer.

VASP activation via the Galpha13/RhoA/PKA pathway mediates cucurbitacin-B-induced actin aggregation and cofilin-actin rod formation.[Pubmed:24691407]

PLoS One. 2014 Apr 1;9(4):e93547.

Cucurbitacin B (CuB), a potent antineoplastic agent of cucurbitacin triterpenoids, induces rapid disruption of actin cytoskeleton and aberrant cell cycle inhibiting carcinogenesis. However, the underlying molecular mechanism of such anticancer effects remains incompletely understood. In this study, we showed that CuB treatment rapidly induced vasodilator-stimulated phosphoprotein (VASP) phosphorylation (i.e. activation) at the Ser157 residue and generated VASP clumps which were co-localized with amorphous actin aggregates prior to the formation of highly-ordered cofilin-actin rods in melanoma cells. Knockdown of VASP or inhibition of VASP activation using PKA-specific inhibitor H89 suppressed CuB-induced VASP activation, actin aggregation and cofilin-actin rod formation. The VASP activation was mediated by cAMP-independent PKA activation as CuB decreased the levels of cAMP while MDL12330A, an inhibitor of adenylyl cyclase, had weak effect on VASP activation. Knockdown of either Galpha13 or RhoA not only suppressed VASP activation, but also ameliorated CuB-induced actin aggregation and abrogated cofilin-actin rod formation. Collectively, our studies highlighted that the CuB-induced actin aggregation and cofilin-actin rod formation was mediated via the Galpha13/RhoA/PKA/VASP pathway.

Cucurbitacin-B inhibits neuroblastoma cell proliferation through up-regulation of PTEN.[Pubmed:25487942]

Eur Rev Med Pharmacol Sci. 2014;18(21):3297-303.

OBJECTIVE: Cucurbitacins belong to a class of highly oxidized tetracyclic triterpenoids. Recent studies suggest that the use of Cucurbitacin could repress cancer cell progression. However, the biological effect of Cucurbitacin-B in neuroblastoma cells remains unexplored. MATERIALS AND METHODS: MTT and BrdU (bromodeoxyuridine) incorporation assays were used to determine the anti-proliferation roles of Cucurbitacin-B. Real-time PCR and Western blot assays were used to detect the expression of cell cycle regulators. Small interfering RNAs (siRNAs) were used to silence the expression of PTEN (phosphatase and tensin homolog gene). RESULTS: We found that Cucurbitacin-B inhibited growth and modulated expression of cell-cycle regulators in SHSY5Y cells. At the molecular level, we found that Cucurbitacin-B inhibited AKT signaling activation through up-regulation of PTEN. Indeed, PTEN deficiency using siRNA oligos attenuated the anti-proliferative roles of Cucurbitacin-B. CONCLUSIONS: These results provide evidence for a mechanism that may contribute to the antineoplastic effects of Cucurbitacin-B in neuroblastoma.

Cucurbitacin B regulates immature myeloid cell differentiation and enhances antitumor immunity in patients with lung cancer.[Pubmed:22746287]

Cancer Biother Radiopharm. 2012 Oct;27(8):495-503.

The aberrant activation of the JAK2/STAT3 signaling in immature myeloid dendritic cells (DCs) is associated with immune tolerance and poor antitumor immunity. The objective of this study was to test the hypothesis that Cucurbitacin B (CuB), a selective inhibitor of JAK2/STAT3 signaling, could promote DC differentiation and improve antitumor immunity. Twelve patients with advanced lung cancers were treated orally with CuB daily for 7 consecutive days. The frequency of peripheral blood myeloid DCs and immature myeloid cells (imCs) in those patients and healthy controls was characterized longitudinally by flow cytometry. The effect of CuB on the differentiation of DCs and p53-specific T responses was evaluated in vitro. The percentages of Lin(-)DR(-)CD33(+) imCs and Lin(-)DR(+)CD33(+) DCs were significantly different between patients with lung cancers and healthy controls (1.55% vs. 0.82%, p=0.002; 0.60% vs. 1.90%, p=0.000). Treatment with CuB significantly increased the frequency of Lin(-)DR(+)CD33(+), but reduced the frequency of Lin(-)DR(-)CD33(+) in patients with lung cancers (p<0.05). Treatment with CuB induced the differentiation of DCs cocultured with tumor cells 16HBE/BPDE and enhanced the sensitivity of 16HBE/BPDE cells to p53-specific CTL by inhibiting the JAK2/STAT3 activation, but also enhancing the interferon-gamma-related STAT1 activation in 16HBE/BPDE cells. CuB significantly reduced the frequency of imCs in patients with lung cancers and enhanced the effect of p53-specific CTL on tumor 16HBE/BPDE cells.

Cucurbitacin B inhibits the translational expression of hypoxia-inducible factor-1alpha.[Pubmed:24333213]

Eur J Pharmacol. 2014 Jan 15;723:46-54.

Cucurbitacin B is a triterpenoid compound isolated from Trichosanthes kirilowii Maximowicz, which has been used in oriental medicine for its antitumor activities. However, the mechanisms by which Cucurbitacin B inhibits tumor growth are not fully understood. We here demonstrated the effect of Cucurbitacin B on hypoxia-inducible factor-1 (HIF-1) activation. Cucurbitacin B showed the potent inhibitory activity against HIF-1 activation induced by hypoxia in various human cancer cell lines. This compound markedly decreased the hypoxia-induced accumulation of HIF-1alpha protein dose-dependently, whereas it did not affect the expressions of HIF-1beta. Further analysis revealed that Cucurbitacin B inhibited HIF-1alpha protein synthesis, without affecting the expression level of HIF-1alpha mRNA or degradation of HIF-1alpha protein. Rather, we found that suppression of HIF-1alpha accumulation by Cucurbitacin B correlated with strong dephosphorylation of mammalian target of rapamycin (mTOR) and its effectors ribosomal protein S6 kinase (p70S6K) and eukaryotic initiation factor 4E-binding protein-1 (4E-BP1) and extracellular signal-regulated kinase-1/2 (ERK1/2), a pathway known to regulate HIF-1alpha expression at the translational level. Cucurbitacin B also activated Akt, a mechanistic feature exhibited by established mTOR inhibitors in many tumor cells. Furthermore, Cucurbitacin B prevented hypoxia-induced expression of HIF-1 target genes and suppresses the invasiveness of tumor cells. In vivo studies further confirmed the inhibitory effect of Cucurbitacin B on the expression of HIF-1alpha proteins, leading to a decrease growth of HeLa cells in a xenograft tumor model. These results show that Cucurbitacin B is an effective inhibitor of HIF-1 and provide new perspectives into the mechanism of its anticancer activity.

Description

Cucurbitacin B belongs to a class of highly oxidized tetracyclic triterpenoids; could repress cancer cell progression.