Curcumin and cancer: An “old-age” disease with an “age-old” solution

Anand, Preetha; Sundaram, Chitra; Jhurani, Sonia; Kunnumakkara, Ajaikumar B.; Aggarwal, Bharat B.

doi:10.1016/j.canlet.2008.03.025

Cited by 1,002 publications

(712 citation statements)

References 224 publications

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“…Garcinol and anacardic acid are both EP300 and KAT2B HAT inhibitors. Antitumor activities of all the three molecules in a wide variety of cancers include interefernce with different cell signaling pathways, like cell cycle (cyclin D1 and cyclin E), apoptosis (activation of caspases and downregulation of antiapoptotic gene products), proliferation (HER-2, EGFR, and AP-1), survival (PI3K/AKT pathway), invasion (MMP-9 and adhesion molecules), angiogenesis (VEGF), metastasis (CXCR-4) and inflammation (NF-κB, TNF, IL-6, IL-1, COX-2, and 5-LOX) (Anand et al 2008;Wu et al 2011;Ahmad et al 2012). Green tea polyphenols suppresses class I histone deacetylases, and thus causes cell cycle arrest and apoptosis in prostate cancer (Thakur et al 2012).…”

Section: Polyphenolmentioning

confidence: 99%

Epigenetic Modifications: Therapeutic Potential in Cancer

Sachan

Kaur

2015

Braz. arch. biol. technol.

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Epigenetic modifications and alterations in chromatin structure and function contribute to the cumulative changes observed as normal cells undergo malignant transformation. These modifications and enzymes (DNA methyltransferases, histone deacetylases, histone methyltransferases, and demethylases) related to them have been deeply studied to develop new drugs, epigenome-targeted therapies and new diagnostic tools. Epigenetic modifiers aim to restore normal epigenetic modification patterns through the inhibition of epigenetic modifier enzymes. Four of them (azacitidine, decitabine, vorinostat and romidepsin)

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Section: Polyphenolmentioning

confidence: 99%

Epigenetic Modifications: Therapeutic Potential in Cancer

Sachan

Kaur

2015

Braz. arch. biol. technol.

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“…In the last decade a large number of reports have been published on the beneficial effects of curcumin, and it has repeatedly been claimed that this natural product is efficient and safe for the prevention and treatment of several diseases including cancer. [1][2][3] It is not surprising, therefore, that curcumin is currently sold as a dietary supplement and that numerous clinical trials are ongoing or recruiting participants to evaluate curcumin activity. But there is accumulating evidence that curcumin may not be so effective and safe.…”

Section: Dear Editormentioning

confidence: 99%

“…8 Although this letter is focused on the negative properties of curcumin, it is important to note that there is evidence suggesting that curcumin has beneficial properties and could be developed into a drug for the prevention and treatment of diseases such as cancer. [1][2][3][4] There are indeed numerous reports showing beneficial effects of curcumin in colon cancer, yet a potential role for curcumin in colon cancer has been shown in few clinical studies only. 63 In vivo data suggest that curcumin may also exert beneficial effects in organs outside the gastrointestinal tract; 4 however, since curcumin does not reach these organs at high concentrations, it is not clear at this point whether these beneficial effects are due to low levels of curcumin, to metabolites of curcumin or to an unknown indirect effect.…”

Section: Dear Editormentioning

confidence: 99%

The dark side of curcumin

Burgos-Morón

Calderón-Montaño

Salvador

et al. 2010

Intl Journal of Cancer

303

210

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Dear Editor,Curcumin is a yellow-orange pigment obtained from the plant Curcuma longa. The powdered rhizome of this plant, called turmeric, is a common ingredient in curry powders and has a long history of use in traditional Asian medicine for a wide variety of disorders. In the last decade a large number of reports have been published on the beneficial effects of curcumin, and it has repeatedly been claimed that this natural product is efficient and safe for the prevention and treatment of several diseases including cancer. 1-3 It is not surprising, therefore, that curcumin is currently sold as a dietary supplement and that numerous clinical trials are ongoing or recruiting participants to evaluate curcumin activity. But there is accumulating evidence that curcumin may not be so effective and safe. Because such evidence is not generally acknowledged, the purpose of this letter is to briefly review the negative properties of curcumin so that they can be balanced against its beneficial effects.Most of the evidence that supports the therapeutic potential of curcumin is mainly based on in vitro studies in which curcumin was tested at concentrations in the micromolar range. Several reports have demonstrated, however, that the plasma concentrations of curcumin in people taking relatively high oral doses of this compound are very low, typically in the nanomolar range (reviewed in Ref. 4). For instance, a recent study examined the pharmacokinetics of a curcumin preparation in 12 healthy human volunteers 0.25-72 hr after an oral dose of 10 or 12 g. Using a high-performance liquid chromatography assay with a limit of detection of 50 ng mL À1 , only 1 subject had detectable free curcumin at any of the time points assayed. 5 The fact that curcumin also undergoes extensive metabolism in intestine and liver 6,7 means that high concentrations of curcumin cannot be achieved and maintained in plasma and tissues after oral ingestion. This is a major obstacle for the clinical development of this agent and suggests that the therapeutic potential of oral curcumin is limited. The low clinical efficiency of curcumin in the treatment of several chronic diseases such as Alzheimer's disease and cardiovascular diseases has been discussed recently. 8 As far as cancer is concerned, in vitro studies have demonstrated that cancer cells do not die unless they are exposed to curcumin concentrations of 5-50 lM for several hours. 4,9,10 Because of its poor bioavailability, these concentrations are not achieved outside the gastrointestinal tract when curcumin is taken orally. Because of its extensive metabolism in intestine and liver, these concentrations cannot be maintained for several hours in the gastrointestinal tract. This suggests that the chemotherapeutic potential of oral curcumin is limited even for the treatment of cancers of the gastrointestinal tract. Accordingly, when 15 patients with advanced colorectal cancer were treated with curcumin at daily doses of 3.6 g for up to 4 months, no partial responses to treatment or decreases in tu...

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“…Curcumin, a type of yellow pigment that is extracted from the rhizome of turmeric, has been used for centuries as a food additive and a traditional medicine in Asian countries [3] . Recently, curcumin gained attention as an anti-cancer agent due to its chemopreventive and chemotherapeutic potential, while having no discernable side effects [4,5] . The molecular mechanisms underlying the anticancer effects of curcumin have been studied in some detail, but are not completely understood.…”

Section: Introductionmentioning

confidence: 99%

Curcumin inhibits AP-2γ-induced apoptosis in the human malignant testicular germ cells in vitro

Zhou

Zhao

et al. 2013

Acta Pharmacol Sin

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Aim: To investigate the effects of curcumin on proliferation and apoptosis in testicular cancer cells in vitro and to investigate its molecular mechanisms of action. Methods: NTera-2 human malignant testicular germ cell line and F9 mouse teratocarcinoma stem cell line were used. The anti-proliferative effect was examined using MTT and colony formation assays. Hoechst 33258 staining, TUNEL and Annexin V-FITC/PI staining assays were used to analyze cell apoptosis. Protein expression was examined with Western blot analysis and immunocytochemical staining. Results: Curcumin (5, 10 and 15 μmol/L) inhibited the viability of NTera-2 cells in dose-and time-dependent manners. Curcumin significantly inhibited the colony formation in both NTera-2 and F9 cells. Curcumin dose-dependently induced apoptosis of NTera-2 cells by reducing FasL expression and Bcl-2-to-Bax ratio, and activating caspase-9, -8 and -3. Furthermore, curcumin dose-dependently reduced the expression of AP transcription factor AP-2γ in NTera-2 cells, whereas the pretreatment with the proteasome inhibitor MG132 blocked both the curcumin-induced reduction of AP-2γ and antiproliferative effect. Curcumin inhibited ErbB2 expression, and decreased the phosphorylation of Akt and ERK in NTera-2 cells. Conclusion: Curcumin induces apoptosis and inhibits proliferation in NTera-2 cells via the inhibition of AP-2γ-mediated downstream cell survival signaling pathways.

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Curcumin and cancer: An “old-age” disease with an “age-old” solution

Cited by 1,002 publications

References 224 publications

Epigenetic Modifications: Therapeutic Potential in Cancer

Epigenetic Modifications: Therapeutic Potential in Cancer

The dark side of curcumin

Curcumin inhibits AP-2γ-induced apoptosis in the human malignant testicular germ cells in vitro

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