Quantitative cellular uptake, localization and cytotoxicity of curcumin in normal and tumor cells

Kunwar, Amit; Barik, Atanu; Mishra, Beena; Rathinasamy, Krishnan; Pandey, R.; Priyadarsini, K. Indira

doi:10.1016/j.bbagen.2007.11.016

Cited by 314 publications

(237 citation statements)

References 26 publications

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“…Although Curcumin has been extensively investigated as it concerns its anti-cancer activity in a variety of cell types, only few studies provide uptake data [33,34] and none correlates kinetic stability of natural and synthetic Curcuminoids to their cellular uptake. A preliminary kinetic study was performed for bDMC and DAC (Fig.…”

Section: Uptake Of Curcumin and Its Derivatives In Hct116 Cellsmentioning

confidence: 99%

Curcumin derivatives: Molecular basis of their anti-cancer activity

Basile

Ferrari

Lazzari

et al. 2009

Biochemical Pharmacology

161

126

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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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Section: Uptake Of Curcumin and Its Derivatives In Hct116 Cellsmentioning

confidence: 99%

Curcumin derivatives: Molecular basis of their anti-cancer activity

Basile

Ferrari

Lazzari

et al. 2009

Biochemical Pharmacology

161

126

View full text Add to dashboard Cite

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“…In one of the recent papers it was found that, except for membrane localization, minor nuclear localization occurred in mouse spleen lymphocytes, mouse fibroblast (NIH3T3), T cell lymphoma of murine origin (EL4) and breast cancer cell line of human origin (MCF7) (Kunwar et al, 2008). Cytotoxicity study on these cell lines indicated that curcumin toxicity in one individual cell line increased with its increased accumulation, but general correlation between accumulation and toxicity was not found.…”

Section: Discussionmentioning

confidence: 99%

“…Curcumin fluorescence is weak in aqueous solutions (Khopde et al, 2000), but in hydrophobic micelles it is enhanced by nearly 55 times (Wang et al, 2006). Since curcumin is a lipophilic compound and accumulates mainly in the membranes (Kunwar et al, 2008), its accumulation in hydrophobic parts of membranes probably explains significant fluorescence that was detected by flow cytometry. The presence of extracellularly bound curcumin is probably not detected due to its weak florescence in aqueous solutions.…”

Section: Curcumin Accumulation In Hep-2 and 7t Cellsmentioning

confidence: 99%

Carboplatin resistant human laryngeal carcinoma cells are cross resistant to curcumin due to reduced curcumin accumulation

Rak

Čimbora‐Zovko

Gajski

et al. 2013

Toxicology in Vitro

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“…Considering that uptake of curcumin by malignant cells seems to be higher than by normal cells, a preferential action of curcumin toward tumor than healthy tissue might be expected. 24 Chang et al 25 compared the in vitro cytotoxicity of curcumin in MG-63 osteosarcoma and healthy human osteoblasts treated at different concentrations (5, 10, 25, 50, 75 and 100 mM). Treatment with 10 mM curcumin reduced viability of MG-63 osteosarcoma cells by 50% as compared with the untreated control.…”

Section: Pathological Bone Environmentmentioning

confidence: 99%

Therapeutic actions of curcumin in bone disorders

2016

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Curcumin is the active component of turmeric extract derived from the Curcuma longa plant. In the last decade, curcumin has raised a considerable interest in medicine owing to its negligible toxicity and multiple therapeutic actions including anti-cancer, anti-inflammatory and anti-microbial activities. Among the various molecular targets of curcumin, some are involved in bone remodeling, which strongly suggests that curcumin can affect the skeletal system. The review sheds light on the current and potential applications of curcumin to treat bone disorders characterized by an excessive resorption activity. Within the scope of this review, the novel formulations of curcumin to overcome its physico-chemical and pharmacokinetic constraints are also discussed.

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Quantitative cellular uptake, localization and cytotoxicity of curcumin in normal and tumor cells

Cited by 314 publications

References 26 publications

Curcumin derivatives: Molecular basis of their anti-cancer activity

Curcumin derivatives: Molecular basis of their anti-cancer activity

Carboplatin resistant human laryngeal carcinoma cells are cross resistant to curcumin due to reduced curcumin accumulation

Therapeutic actions of curcumin in bone disorders

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