Curcumin: a new cell-permeant inhibitor of the inositol 1,4,5-trisphosphate receptor

Dyer, Jeanette L.; Khan, Shahla Zafar; Bilmen, Jonathan G.; Hawtin, Stuart R.; Wheatley, Mark; Javed, Masood-Ul-Hassan; Michelangeli, Francesco

doi:10.1054/ceca.2001.0259

Cited by 48 publications

(29 citation statements)

References 31 publications

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“…3A and B). Several studies have shown that curcumin suppresses Ca 2+ activation by a variety of stimuli (35,36); therefore, we examined the effects of curcumin on Ca 2+ signaling changes in HCT116 cells (Fig. 5C and D).…”

Section: Resultsmentioning

confidence: 99%

Curcumin Inhibits Neurotensin-Mediated Interleukin-8 Production and Migration of HCT116 Human Colon Cancer Cells

Wang¹,

Wang²,

Ives³

et al. 2006

Clinical Cancer Research

101

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Purpose: Neurotensin, a gut tridecapeptide, acts as a potent cellular mitogen for various colorectal and pancreatic cancers that possess high-affinity neurotensin receptors. Cytokine/ chemokine proteins are increasingly recognized as important local factors that play a role in the metastasis and invasion of multiple cancers. The purpose of this study was to (a) determine the effect of neurotensin on cytokine/chemokine gene expression and cell migration in human cancer cells and (b) assess the effect of curcumin, a natural dietary product, on neurotensinmediated processes. Experimental Design: The human colorectal cancer, HCT116, was treated with neurotensin, with or without curcumin, and interleukin (IL)-8 expression and protein secretion was measured. Signaling pathways, which contribute to the effects of neurotensin, were assessed. Finally, the effect of curcumin on neurotensin-mediated HCT116 cell migration was analyzed. Results: We show that neurotensin, acting through the native high-affinity neurotensin receptor, induced IL-8 expression in human colorectal cancer cells in a time-and dose-dependent fashion. This stimulation involves Ca 2+ -dependent protein kinase C, extracellular signal-regulated kinased ependent activator protein-1, and extracellular signal-regulated kinase^independent nuclear factor-nB pathways. Curcumin inhibited neurotensin-mediated activator protein-1 and nuclear factor-nB activation and Ca 2+ mobilization. Moreover, curcumin blocked neurotensin-stimulated IL-8 gene induction and protein secretion and, at a low concentration (i.e., 10 Amol/L), blocked neurotensin-stimulated colon cancer cell migration. Conclusions: Neurotensin-mediated induction of tumor cell IL-8 expression and secretion may contribute to the procarcinogenic effects of neurotensin on gastrointestinal cancers. Furthermore, a potential mechanism for the chemopreventive and chemotherapeutic effects of curcumin on colon cancers may be through the inhibition of gastrointestinal hormone (e.g., neurotensin)î nduced chemokine expression and cell migration.

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Section: Resultsmentioning

confidence: 99%

Curcumin Inhibits Neurotensin-Mediated Interleukin-8 Production and Migration of HCT116 Human Colon Cancer Cells

Wang¹,

Wang²,

Ives³

et al. 2006

Clinical Cancer Research

101

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“…In human HCT-116 colon cancer cells, the tumorpropagating effects of neurotensin could be deterred by curcumin treatment (10-25 mM), which conceivably hindered cPKC activation by inhibiting the release of Ca 2+ from the ER (Dyer et al, 2002;Wang et al, 2006a). Corroboratively, curcumin (20 mM) impaired PKC activity in human astroglioma cells stimulated with the PKC agonist TPA (Woo et al, 2005).…”

Section: +mentioning

confidence: 99%

The Molecular Basis for the Pharmacokinetics and Pharmacodynamics of Curcumin and Its Metabolites in Relation to Cancer

Golen²,

et al. 2013

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“…Yeon et al reported that curcumin inhibits neuronal TRPV1 (IC 50 , 67 nM) that are known to mediate pain and thermal sensation (16). Also, the InsP 3 receptors in ER membrane are inhibited by curcumin (IC 50 , 10 μM), indicating another mechanism affecting the cellular Ca 2+ signal (17). Considering the lipophilicity, curcumin might nonspecifically inhibit the channels via dissolving into the plasma membrane or through a chemical modification of ion channels.…”

Section: Wide Spectrum Of Ion Channel Modulating Effects By Curcuminmentioning

confidence: 99%

Inhibition of Ca2+-Release–Activated Ca2+ Channel (CRAC) and K+ Channels by Curcumin in Jurkat-T Cells

et al. 2011

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Abstract. The increase in cytoplasmic Ca] c of Jurkat-T cells using the patch clamp technique and fura-2 spectrofluorimetry. Curcumin (10 μM) inhibited store-operated Ca 2+ entry (SOCE). Consistently, dose-dependent inhibition of I CRAC by curcumin was confirmed in Jurkat-T (IC 50 , 5.9 μM) and the HEK293 cells overexpressing Orai1 and STIM1 (IC 50 , 0.6 μM). Also, curcumin inhibited both I Kv (IC 50 , 11.9 μM) and I SK4 (IC 50 , 4.2 μM). The other polyphenols (rosmarinic acid, resveratrol, and epigallocatechin gallate at 10 -30 μM) had no effect on SOCE and showed only a partial inhibition of the K + currents. In summary, among the tested polyphenolic agents, curcumin showed prominent inhibition of major ion channels in lymphocytes, which might contribute to the anti-inflammatory effects of curcumin.

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Curcumin: a new cell-permeant inhibitor of the inositol 1,4,5-trisphosphate receptor

Cited by 48 publications

References 31 publications

Curcumin Inhibits Neurotensin-Mediated Interleukin-8 Production and Migration of HCT116 Human Colon Cancer Cells

Curcumin Inhibits Neurotensin-Mediated Interleukin-8 Production and Migration of HCT116 Human Colon Cancer Cells

The Molecular Basis for the Pharmacokinetics and Pharmacodynamics of Curcumin and Its Metabolites in Relation to Cancer

Inhibition of Ca2+-Release–Activated Ca2+ Channel (CRAC) and K+ Channels by Curcumin in Jurkat-T Cells

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