Inhibitory effects of curcumin on protein kinase C activity induced by 12-<i>O</i>-tetradecanoyl-phorbol-13-acetate in NIH 3T3 cells

Liu, Jer Yuh; Lin, Su; Lin, Ju‐Li

doi:10.1093/carcin/14.5.857

Cited by 245 publications

(161 citation statements)

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“…Immunoprecipitated CFTR was washed three times with ice-cold lysis buffer containing detergent and once with lysis buffer without detergent. Pellets were then phosphorylated with 40 nM catalytic subunits of PKA (Promega, Madison, WI) and [␥- 32 P]ATP (6000 Ci/mM, PerkinElmer Life Sciences) plus the indicated concentrations of curcumin or the Me 2 SO vehicle control. Phosphorylation was stopped by dilution into 100ϫ volume of lysis buffer and cAMP-dependent protein kinase peptide inhibitor (PKI) (10 M) (Promega).…”

Section: Methodsmentioning

confidence: 99%

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Curcumin Stimulates Cystic Fibrosis Transmembrane Conductance Regulator Cl– Channel Activity

Berger¹,

Randak²,

Ostedgaard³

et al. 2005

Journal of Biological Chemistry

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Compounds that enhance either the function or biosynthetic processing of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl ؊ channel may be of value in developing new treatments for cystic fibrosis (CF). Previous studies suggested that the herbal extract curcumin might affect the processing of a common CF mutant, CFTR-⌬F508. Here, we tested the hypothesis that curcumin influences channel function. Curcumin increased CFTR channel activity in excised, inside-out membrane patches by reducing channel closed time and prolonging the time channels remained open. Stimulation was dose-dependent, reversible, and greater than that observed with genistein, another compound that stimulates CFTR. Curcumin-dependent stimulation required phosphorylated channels and the presence of ATP. We found that curcumin increased the activity of both wild-type and ⌬F508 channels. Adding curcumin also increased Cl ؊ transport in differentiated non-CF airway epithelia but not in CF epithelia. These results suggest that curcumin may directly stimulate CFTR Cl ؊ channels.

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Section: Methodsmentioning

confidence: 99%

“…2). Curcumin has also been reported to inhibit protein kinase C activity (32). The reduced PKA activity may explain, in part, the decreasing current in response to high curcumin concentrations in the presence of PKA.…”

Section: Curcumin Stimulates Cftr In Excised Membranementioning

confidence: 99%

Curcumin Stimulates Cystic Fibrosis Transmembrane Conductance Regulator Cl– Channel Activity

Berger¹,

Randak²,

Ostedgaard³

et al. 2005

Journal of Biological Chemistry

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“…16 Both flavonoids (e.g., apigenin) and phenolic acid analogs (e.g., curcumin) (Tables I and III, respectively) are effective at inhibiting signal transduction enzymes, such as PKC 33 or tyrosine kinases (PTK). 34 For instance, curcumin inhibits PKC activity in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced NIH 3T3 cells 35 (see Table I). The stilbene resveratrol (Table II) has also been reported as implicated in the regulation of apoptosis, probably by inhibiting PKC activity in human gastric adenocarcinoma KATO-III cells.…”

Section: Suppression Of Protein Kinases (Pks)mentioning

confidence: 99%

New insights on the anticancer properties of dietary polyphenols

et al. 2006

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Cancer, one of the major causes of death across the world, has shown to be a largely preventable disease, highly susceptible to modulation by dietary factors. Phenolic compounds, abundant in vegetables and fruits ubiquitous in diet, were described to play an important role as chemopreventive agents. Since conventional therapeutic and surgical approaches have not been able to control the incidence of most cancer types, the development of chemopreventive strategies is an urgent priority in public health. The current diet phenolic intake is often insufficient to protect from mutagens (either exogenous or endogenous), which leads to the need for dietary supplementation as an alternative approach. Research efforts are placing increasing emphasis on identifying the biological mechanisms and in particular the signal transduction pathways related to the chemopreventive activities of these compounds. These effects are believed to occur by the regulation of signaling pathways such as nuclear factor-kB (NF-kB), activator protein-1 (AP-1) or mitogen-activated protein kinases (MAPK). Dietary polyphenols can exert their effects on these pathways separately or sequentially and in addition the occurrence of crosstalk between these pathways cannot be overlooked. By modulating cell signaling pathways, polyphenols activate cell death signals and induce apoptosis in precancerous or malignant cells resulting in the inhibition of cancer development or progression. However, regulation of cell signaling pathways by dietary polyphenols can also lead to cell proliferation/survival or inflammatory responses due to increased expression of several genes. The present review summarizes the most recent advances providing new insights into the molecular mechanisms underlying the promising anticarcinogenic activity of dietary polyphenols. ß

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“…Among various naturally occurring phytochemicals, curcumin is capturing the attention of cancer investigators worldwide because of its chemo-preventive properties against human malignancies (18 -20). The anti-carcinogenic properties of curcumin in animals have been demonstrated by its inhibition of tumor initiation induced by various carcinogens (21,22). This yellow pigment interrupts cell cycle, disrupts mitotic spindle structure, and induces micro-nucleation, thereby acting as anti-proliferative agent in various cancer cells (23).…”

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confidence: 99%

Curcumin Selectively Induces Apoptosis in Deregulated Cyclin D1-expressed Cells at G2 Phase of Cell Cycle in a p53-dependent Manner

Choudhuri

Pal

Das

et al. 2005

Journal of Biological Chemistry

289

226

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Curcumin (diferuloylmethane) is known to induce apoptosis in tumor cells. In asynchronous cultures, with time-lapse video-micrography in combination with quantitative fluorescence microscopy, we have demonstrated that curcumin induces apoptosis at G 2 phase of cell cycle in deregulated cyclin D1-expressed mammary epithelial carcinoma cells, leaving its normal counterpart unaffected. In our search toward delineating the molecular mechanisms behind such differential activities of curcumin, we found that it selectively increases p53 expression at G 2 phase of carcinoma cells and releases cytochrome c from mitochondria, which is an essential requirement for apoptosis. Further experiments using p53-null as well as dominant-negative and wildtype p53-transfected cells have established that curcumin induces apoptosis in carcinoma cells via a p53-dependent pathway. On the other hand, curcumin reversibly inhibits normal mammary epithelial cell cycle progression by down-regulating cyclin D1 expression and blocking its association with Cdk4/Cdk6 as well as by inhibiting phosphorylation and inactivation of retinoblastoma protein. In addition, curcumin significantly up-regulates cell cycle inhibitory protein (p21Waf-1) in normal cells and arrests them in G 0 phase of cell cycle. Therefore, these cells escape from curcumin-induced apoptosis at G 2 phase. Interestingly, these processes remain unaffected by curcumin in carcinoma cells where cyclin D1 expression is high. Similarly, in ectopically overexpressed system, curcumin cannot down-regulate cyclin D1 and thus block cell cycle progression. Hence, these cells progress into G 2 phase and undergo apoptosis. These observations together suggest that curcumin may have a possible therapeutic potential in breast cancer patients.

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Inhibitory effects of curcumin on protein kinase C activity induced by 12-O-tetradecanoyl-phorbol-13-acetate in NIH 3T3 cells

Cited by 245 publications

References 0 publications

Curcumin Stimulates Cystic Fibrosis Transmembrane Conductance Regulator Cl– Channel Activity

Curcumin Stimulates Cystic Fibrosis Transmembrane Conductance Regulator Cl– Channel Activity

New insights on the anticancer properties of dietary polyphenols

Curcumin Selectively Induces Apoptosis in Deregulated Cyclin D1-expressed Cells at G2 Phase of Cell Cycle in a p53-dependent Manner

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