Selective Modulation of Protein Kinase A and Protein Kinase C Activities in Epidermal Growth Factor (EGF)-Stimulated MCF-7 Breast Cancer Cells

Mueller, Heinz; Liu, Rong; David, Françoise; Eppenberger, Urs

doi:10.1515/bchm.1997.378.9.1023

Cited by 17 publications

(13 citation statements)

References 36 publications

(16 reference statements)

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“…It was reported that PKA in MCF-7 cells is ac- . [16,17] As shown in Figures 3 E and S7, the activation of PKA in MCF-7 cells by these drugs was clearly detected through color changes in the GNP dispersions.…”

mentioning

confidence: 87%

Measurement of Homogeneous Kinase Activity for Cell Lysates Based on the Aggregation of Gold Nanoparticles

et al. 2007

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mentioning

confidence: 87%

Measurement of Homogeneous Kinase Activity for Cell Lysates Based on the Aggregation of Gold Nanoparticles

et al. 2007

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“…To investigate whether these signals are required for DIM-induced JNK and p38 activation and IFNg expression in MCF-7 cells, we examined the effects of inhibitors of PKC and Ca 2 þ -dependent pathways on expression of the pIFN-108 reporter construct. Results shown in Figure 9a indicated that treatment with four different PKC inhibitors, GF109203X (Kiang et al, 1999), Go¨6983 (Cui et al, 2003), Calphostin C (Rosfjord et al, 1999), and Chelerythrine (Mueller et al, 1997), did not affect the inducing effect of DIM on IFNg transcription. GF109203X and Go¨6983 are general inhibitors of cPKC and nPKC kinase activities.…”

Section: Inhibition Of Ca 2 þ -Dependent Pathways Significantly Blockmentioning

confidence: 97%

DIM stimulates IFNγ gene expression in human breast cancer cells via the specific activation of JNK and p38 pathways

2005

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3,30 -Diindolylmethane (DIM) is a promising anticancer agent derived from Brassica vegetables, but the mechanisms of DIM action are largely unknown. We have shown that DIM can upregulate the expression and stimulate the secretion of interferon-gamma (IFNc) in the human MCF-7 breast cancer cell line. This novel effect may provide important clues to explain the anticancer effects of DIM because it is well known that IFNc plays an important role in preventing the development of primary and transplanted tumors. Utilizing promoter deletions, we show here that the region between À108 and À36 bp in the IFNc promoter, which contains two conserved and essential regulatory elements, is required for DIM-induced IFNc expression. DIM activates both JNK and p38 pathways, induces the phosphorylation of c-Jun and ATF-2, and increases the binding of the homodimer or heterodimer of c-Jun/ATF-2 to the proximal AP-1 . CREB-ATF-binding element. Moreover, studies with specific enzyme inhibitors showed that up-stream Ca 2 þ -dependent kinase(s) is required for the inducing effects of DIM in MCF-7 cells. These results establish that DIM-induced IFNc expression in human breast tumor cells is mediated by activation of both JNK and p38 pathways, which is ultimately dependent on intracellular calcium signaling.

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“…The activation of the mitogen-activated protein (MAP) kinase cascade seems to be the most prominent pathway, which is triggered by TGF-␣ in the CNS. Apart from MAP kinase activation, PLC-␥-dependent protein kinase C (PKC), as well as phosphatidylinositol 3-kinase (PI3-kinase), are also targeted by EGF receptor agonists (Mueller et al, 1997;Moghal and Sternberg, 1999). Using specific inhibitors of MEK1/2 (U0126, 10 M), PKC (Gö6983, 1 M), as well as PI3-kinase (LY294002, 10 M), the role of these pathways in the regulation of caveolin-1 was elucidated.…”

Section: Inhibition Of the Pi3-kinase As Well As Histone Deacetylasesmentioning

confidence: 99%

Caveolin and GLT‐1 gene expression is reciprocally regulated in primary astrocytes: Association of GLT‐1 with non‐caveolar lipid rafts

Zschocke

Bayatti

Behl

2004

Glia

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Caveolae represent membrane microdomains acting as integrators of cellular signaling and functional processes. Caveolins are involved in the biogenesis of caveolae and regulate the activity of caveolae-associated proteins. Although caveolin proteins are found in the CNS, the regulation of caveolins in neural cells is poorly described. In the present study, we investigated different modes and mechanisms of caveolin gene regulation in primary rat astrocytes. We demonstrated that activation of cAMP-dependent signaling pathways led to a marked reduction in protein levels of caveolin-1/-2 in cortical astrocytes. Application of transforming growth factor-alpha (TGF-alpha) also resulted in a decrease of caveolin-1/-2 expression. Decreased caveolin protein levels were mirrored by diminished caveolin gene transcription. The repressive effect of TGF-alpha on caveolin-1 expression was MAP kinase-independent and partly mediated through the PI3-kinase pathway. Further downstream, inhibition of histone deacetylases abrogated TGF-alpha effects, suggesting that chromatin remodeling processes could contribute to caveolin-1 repression. Intriguingly, alterations of caveolin gene expression in response to cAMP or TGF-alpha coincided with reciprocal and brain-region specific changes in glial glutamate transporter GLT-1 expression. The reciprocal regulation of caveolin-1 and GLT-1 expression might be gated through a common PI3-kinase dependent pathway triggered by TGF-alpha. Finally, we showed that GLT-1 is located in non-caveolar lipid rafts of cortical astrocytes. In conclusion, this study highlights the occurrence of the reciprocal regulation of caveolin and GLT-1 expression during processes such as astrocyte differentiation via common signaling pathways. We also provide strong evidence that GLT-1 itself is concentrated in lipid rafts, inferring an important role for glial glutamate transporter function.

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Selective Modulation of Protein Kinase A and Protein Kinase C Activities in Epidermal Growth Factor (EGF)-Stimulated MCF-7 Breast Cancer Cells

Cited by 17 publications

References 36 publications

Measurement of Homogeneous Kinase Activity for Cell Lysates Based on the Aggregation of Gold Nanoparticles

Measurement of Homogeneous Kinase Activity for Cell Lysates Based on the Aggregation of Gold Nanoparticles

DIM stimulates IFNγ gene expression in human breast cancer cells via the specific activation of JNK and p38 pathways

Caveolin and GLT‐1 gene expression is reciprocally regulated in primary astrocytes: Association of GLT‐1 with non‐caveolar lipid rafts

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