Cardamonin Suppresses the Proliferation of Colon Cancer Cells by Promoting β-Catenin Degradation

Park, Seoyoung; Gwak, Jungsug; Han, Seung Jin; Oh, Sangtaek

doi:10.1248/bpb.b13-00158

Cited by 55 publications

(37 citation statements)

References 26 publications

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“…These results can be correlated with other reports of important cytotoxic effects of these flavonoids [31,32]. Others chalcones possess apoptotic and antiproliferative effects [33,34,35]. …”

Section: Discussionsupporting

confidence: 90%

Derricin and Derricidin Inhibit Wnt/β-Catenin Signaling and Suppress Colon Cancer Cell Growth In Vitro

et al. 2015

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Overactivation of the Wnt/β-catenin pathway in adult tissues has been implicated in many diseases, such as colorectal cancer. Finding chemical substances that can prevent this phenomenon is an emerging problem. Recently, several natural compounds have been described as Wnt/β-catenin inhibitors and might be promising agents for the control of carcinogenesis. Here, we describe two natural substances, derricin and derricidin, belonging to the chalcone subclass, that show potent transcriptional inhibition of the Wnt/β-catenin pathway. Both chalcones are able to affect the cell distribution of β-catenin, and inhibit Wnt-specific reporter activity in HCT116 cells and in Xenopus embryos. Derricin and derricidin also strongly inhibited canonical Wnt activity in vitro, and rescued the Wnt-induced double axis phenotype in Xenopus embryos. As a consequence of Wnt/β-catenin inhibition, derricin and derricidin treatments reduce cell viability and lead to cell cycle arrest in colorectal cancer cell lines. Taken together, our results strongly support these chalcones as novel negative modulators of the Wnt/β-catenin pathway and colon cancer cell growth in vitro.

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Section: Discussionsupporting

confidence: 90%

Derricin and Derricidin Inhibit Wnt/β-Catenin Signaling and Suppress Colon Cancer Cell Growth In Vitro

et al. 2015

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“…Cisplatin was able to induce G2/M arrest in ovarian cancer cells (37,38). A previous study demonstrated that cardamonin inhibits cell growth and induces cell cycle arrest at the G2/M phase in colon cancer SW480 cells by suppressing the expression of cyclin D1, and c-myc (39). The results of the present study revealed that cardamonin increased the accumulation of cells in the S and G2/M phase, and the combination of cardamonin and cisplatin significantly increased the cisplatin-induced G2/M arrest, which indicated that the potential anti-proliferative effect of cardamonin was associated with cell cycle arrest.…”

Section: Discussionmentioning

confidence: 90%

Cardamonin enhances the anti-proliferative effect of cisplatin on ovarian cancer

et al. 2018

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Abstract. The mammalian target of rapamycin (mTOR) is well-known as a promising therapeutic target in various cancer cells. mTOR activation decreases the sensitivity of ovarian cancer to cisplatin. Cardamonin inhibits the proliferation of various cancer cells by mTOR suppression. The present study examined whether cardamonin combined with cisplatin is efficacious for the anti-proliferation of ovarian cancer cells. The anti-proliferative effect was determined by MTT and cell cycle assays. Activation of the mTOR signal pathway and the expression of anti-apoptotic proteins were evaluated by western blot analysis. Cardamonin significantly enhanced the effects of cisplatin on cell proliferation and cell cycle progression. The expression of B cell lymphoma-2, X-linked inhibitor of apoptosis protein and Survivin was significantly decreased following combination treatment. Furthermore, the activation of mTOR and its downstream 70 kDa ribosomal protein S6 kinase was inhibited by cardamonin. These results demonstrated that the combinatorial effects of cardamonin and cisplatin on anti-proliferation were enhanced by suppressing the expression of anti-apoptotic proteins and activation of mTOR in ovarian cancer cells.

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“…Interestingly, cardamonin has been shown to be a potential anti-tumor agent against colon cancer by suppressing the proliferation of cancer cells (22). Thus the anti-tumor properties of cardamonin increase its promising medicinal value for patients with long-standing UC because the most important clinical issue for patients with longstanding UC is an increased risk for the development of colon cancer (25).…”

Section: Discussionmentioning

confidence: 99%

The anti-inflammatory effect and potential mechanism of cardamonin in DSS-induced colitis

Ren

Sun

Deng

et al. 2015

American Journal of Physiology-Gastrointestinal and Liver Physi

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Cardamonin is a naturally occurring chalcone with strong anti-inflammatory activity. However, the direct effect of cardamonin on intestinal inflammation remains elusive. In the present study, we found that cardamonin markedly ameliorated dextran sulfate sodium-induced mouse body weight loss, diarrhea, colon shortening, spleen swelling, and histological damage, which correlated with a decline in the activity of myeloperoxidase and the production of nitric oxide, tumor necrosis factor-α and interleukin-6 in the colon. The upregulation of toll-like receptor 4 after dextran sulfate sodium treatment was associated with an increase in the activation of myeloid differentiation factor 88, interleukin-1 receptor-associated kinase-1, nuclear factor-κB (NF-κB) p65, inhibitor κBα, and inhibitor κB kinase-α/β, as well as the mitogen-activated protein kinase molecules of extracellular signal-regulated kinase and c-Jun NH2-terminal kinase, and this upregulation was reversed by cardamonin administration. Moreover, cardamonin blocked the nuclear translocation of NF-κB p65, inhibited NF-κB-luciferase activity, and downregulated NF-κB target genes expression. The present study clearly demonstrates a beneficial effect of cardamonin on experimental inflammatory bowel disease via a mechanism associated with suppression of toll-like receptor 4 expression and inactivation of NF-κB and mitogen-activated protein kinase pathways. This study may give insight into the further evaluation of the therapeutic potential of cardamonin or its derivatives for human inflammatory bowel disease.

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Cardamonin Suppresses the Proliferation of Colon Cancer Cells by Promoting β-Catenin Degradation

Cited by 55 publications

References 26 publications

Derricin and Derricidin Inhibit Wnt/β-Catenin Signaling and Suppress Colon Cancer Cell Growth In Vitro

Derricin and Derricidin Inhibit Wnt/β-Catenin Signaling and Suppress Colon Cancer Cell Growth In Vitro

Cardamonin enhances the anti-proliferative effect of cisplatin on ovarian cancer

The anti-inflammatory effect and potential mechanism of cardamonin in DSS-induced colitis

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