Curcumin Induces Apoptosis and Inhibits Growth of Human Burkitt’s Lymphoma in Xenograft Mouse Model

Li, Zaixin; Ouyang, Keqing; Jiang, Xv; Wang, Dong; Hu, Yinghe

doi:10.1007/s10059-009-0036-9

Cited by 25 publications

(17 citation statements)

References 49 publications

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“…By investigating c-myc, we found that its expression is downregulated in CF-treated cells as compared to the control, suggesting that p53 negatively regulates c-myc. There are reports in the literature supporting our findings showing that apoptosis could be induced through downregulation of c-myc in curcumin treated cancer cells [28-30]. These data indicate that p53, c-myc, p21 and p27 play a decisive role in CF-induced apoptosis of HCT-116 and MSTO-211 cells.…”

Section: Resultssupporting

confidence: 88%

CELLFOOD™ induces apoptosis in human mesothelioma and colorectal cancer cells by modulating p53, c-myc and pAkt signaling pathways

Nuvoli¹,

Santoro²,

Catalani

et al. 2014

J Exp Clin Cancer Res

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BackgroundCELLFOOD™ (CF) is a nutraceutical non-addictive, non-invasive, and completely non-toxic unique proprietary colloidal-ionic formula. Little is known about its effect on cancer cells in solid tumors. The aim of this study was to evaluate the effect that CF has on different cancer cell lines and the mechanism by which the nutraceutical works.MethodsThe effect of CF on HFF (normal fibroblasts), Met5A (mesothelium), MSTO-211H, NCI-2452, Ist-Mes1, MPP89, Ist-Mes2 (mesothelioma), M14 (melanoma), H1650, H1975 (lung cancer), SKRB3 (breast cancer), and HCT-116 (colorectal cancer) cell growth was tested by cell proliferation and clonogenic assay. Among all of them, MSTO-211 and HCT-116 were analyzed for cell cycle by flow cytometry and western blot.ResultsAll human cancer lines were suppressed on cell growth upon 1:200 CF treatment for 24 and 48 hours. Death was not observed in HFF and Met5A cell lines. Cell cycle analysis showed an increased sub-G1 with reduction of G1 in MSTO-211 and a cell cycle arrest of in G1 in HCT116. Activation of caspase-3 and cleavage of PARP confirmed an apoptotic death for both cell lines. Increased expression levels of p53, p21, and p27, downregulation of c-myc and Bcl-2, and inhibition of Akt activation were also found in CF-treated MSTO-211 and HCT-116 cells.ConclusionsThese findings ascertained an interaction between p53, c-myc, p21, p27, Bcl-2, PI3K/Akt pathway, and CF-induced apoptosis in MSTO-211H and HCT-116 cells, suggesting that CF acts as an important regulator of cell growth in human cancer cell lines. CF could be a useful nutraceutical intervention for prevention in colon cancer and mesothelioma.

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Section: Resultssupporting

confidence: 88%

CELLFOOD™ induces apoptosis in human mesothelioma and colorectal cancer cells by modulating p53, c-myc and pAkt signaling pathways

Nuvoli¹,

Santoro²,

Catalani

et al. 2014

J Exp Clin Cancer Res

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“…Preclinically, it inhibited proliferation of B-cell NHL (B-NHL) cell line Raji cells. Staining showed that curcumin could induce Raji cell apoptosis [76,77]. Multiple ongoing studies are exploring the use of curcumin in vitro with different tumour cell lines and its role in chemoprevention [78].…”

Section: Stat3 Inhibitorsmentioning

confidence: 99%

Epigenetic therapy of lymphoma using histone deacetylase inhibitors

et al. 2010

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In this study, we reviewed epigenetic therapy of lymphomas using histone deacetylase inhibitors (HDACi), a promising new class of antineoplastic agents. Epigenetic therapy, a new therapeutic concept, consists of the use of HDACi and or DNA methyltransferase inhibitors (DNMTi). We conducted a comprehensive review of the literature for antitumour activity of HDACi and its mechanism of action. HDACi modify the expression of several genes related to cancer development, which can result in antineoplastic activity. To elucidate the benefits of HDACi in lymphoma treatment, we discuss the crucial interplay between BCL6, p53 and STAT3. Activated B-cell (ABC) diffuse large cell lymphoma (DLCL) is increasingly being recognised as an unfavourable and frequently therapy-refractory lymphoma. We discuss the fundamental causative role of the STAT3 oncogene in ABC type DLCL. STAT3 can be effectively suppressed by several HDACi, a promising treatment for this difficult subtype of DLCL. On the other hand, various HDACi can repress the germinal-centre B Cell (GCB) type DLCL by virtue of their inhibition of the BCL6 oncogene, usually expressed in this particular subtype. We summarise the results of recent clinical trials with HDACi such as romidepsin, panobinostat, MGCD-0103, entinostat, curcumin, JAK2 inhibitor TG101348, and valproic acid that have shown preliminary activity in recurrent and refractory lymphomas. The unique mechanism of action of HDACi makes them very attractive agents to pursue in combination. Several ongoing trials are already exploring HDACi combinations in various types of cancers. Their role in front-line management remains to be determined.

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“…Curcumin exhibits cancer growth inhibition both in vitro and in vivo [5,6]: it suppresses cell proliferation in a variety of cancer cell lines and it inhibits tumorigenesis [7][8][9][10][11][12][13][14][15][16][17]. Multiple mechanisms of action are likely responsible for Curcumin various effects on cancer cells: G1/S arrest and apoptosis induction have been observed other than the mitotic block in different tumor cell lines [18][19][20].…”

Section: Introductionmentioning

confidence: 99%

Curcumin derivatives: Molecular basis of their anti-cancer activity

Basile

Ferrari

Lazzari

et al. 2009

Biochemical Pharmacology

166

129

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Curcumin, a phenolic compound from the plant Curcuma longa L., has shown a wide-spectrum of chemopreventive, anti-oxidant and anti-tumor properties. Although its promising chemotherapeutic activity, preclinical and clinical studies highlight Curcumin limited therapeutic application due to its instability in physiological conditions. To improve its stability and activity, many derivatives have been synthesized and studied, among which bis-DemethoxyCurcumin (bDMC) and diAcetylCurcumin (DAC). In this report, we show that both bDMC and DAC are more stable than Curcumin in physiological medium. To explore the mechanism of their chemotherapeutic effect, we studied their role in proliferation in the HCT116 human colon cancer cells. We correlated kinetic stability and cellular uptake data to their biological effects. Both bDMC and DAC impair correct spindles formation and induce a p53-and p21 CIP1/WAF1 -independent mitotic arrest, which is more stable and long-lasting for bDMC. A subsequent p53/p21 CIP1/WAF1 -dependent inhibition of G1 to S transition is triggered by Curcumin and DAC as a consequence of the mitotic slippage, preventing postmitotic cells from re-entering the cell cycle. Conversely, the G1/S arrest induced by bDMC is a direct effect of the drug and concomitant to the mitotic block. Finally, we demonstrate that bDMC induces rapid DNA double-strand breaks, moving for its possible development in anti-cancer clinical applications.

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Curcumin Induces Apoptosis and Inhibits Growth of Human Burkitt’s Lymphoma in Xenograft Mouse Model

Cited by 25 publications

References 49 publications

CELLFOOD™ induces apoptosis in human mesothelioma and colorectal cancer cells by modulating p53, c-myc and pAkt signaling pathways

CELLFOOD™ induces apoptosis in human mesothelioma and colorectal cancer cells by modulating p53, c-myc and pAkt signaling pathways

Epigenetic therapy of lymphoma using histone deacetylase inhibitors

Curcumin derivatives: Molecular basis of their anti-cancer activity

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