Rottlerin Stimulates Metallothionein Gene Expression but Inhibits Metal Transport in Chinese Hamster Ovary Cells

Chen, Je-Hsin; Huang, Chiu-Hui; Lin, Lih-Yuan

doi:10.1006/taap.2001.9299

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Cited by 4 publications

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“…The inhibition mechanism for H7, a protein kinase C inhibitor, may be different between the zinc- and cadmium-treated cells. H7 blocks zinc transport but not cadmium transport although rottlerin, a PKC inhibitor that can block both cadmium and zinc transport [21,22]. Hypoxia activates MT expression through the metal response elements and that this activation involves the metal transcription factor-1 (MTF-1) [23].…”

Section: Discussionmentioning

confidence: 99%

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Choi

Cha

et al. 2004

Cancer Cell Int

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Section: Discussionmentioning

confidence: 99%

Untitled

Choi

Cha

et al. 2004

Cancer Cell Int

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Regulation of cadmium-induced apoptosis by PKCδ in U937 human promonocytic cells

Miguel

Rodríguez

Aller

et al. 2005

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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Pulse treatment with cadmium chloride followed by recovery caused apoptosis in U937 human promonocytic cells. In addition, the treatment-induced PKCdelta translocation from cytosol to membrane fraction, which was already detected at 30 min of treatment; and also caused PKCdelta cleavage to give a 41-kDa fragment, which was detected at 3-6 h of recovery, concomitantly with the execution of apoptosis. All these effects were reduced by the PKCdelta-specific inhibitor rottlerin. By contrast, rottlerin did not prevent the cadmium-provoked stimulation of the stress response (as measured by HSP70 expression), nor inhibited the generation of apoptosis by heat-shock, which failed to cause PKCdelta translocation. Cadmium chloride rapidly induced p38(MAPK) activation, which was not affected by rottlerin. By contrast, the p38(MAPK) inhibitor SB203580 reduced PKCdelta translocation and cleavage, indicating that p38(MAPK) activation precedes and regulates PKCdelta activation. It is concluded that PKCdelta mediates apoptosis induction by cadmium ions via early membrane translocation, and also possibly through late kinase proteolytic cleavage and phosphorylation on tyrosine residues.

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