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12-O-tetradecanoylphorbol-13-acetate induces apoptosis in renal epithelial cells through a growth signal conflict which is prevented by activated ras.

Abstract：

:12-O-Tetradecanoylphorbol-13-acetate (TPA) induced apoptosis in the pig renal epithelial cell line LLC-PK1 after 24 h of treatment as assessed by caspase 3 activation. Cotreatment of the cells with bryostatin markedly reduced the apoptotic effects of TPA. Okadaic acid, another tumor promoter, also induced apoptosis. Expression of an activated ras gene prevented TPA-induced apoptosis, while a dominant negative ras retarded the process. Taken together, these results suggest that TPA-induced apoptosis in LLC-PK1 may be analogous to TPA-induced tumor promotion in the two-stage model of skin carcinogenesis. Mechanistically, TPA-induced apoptosis seemed to be the result of a conflict of the growth-promoting affects of serum and the growth-retarding effects of TPA. This was manifested by a pronounced hypophosphorylation of the retinoblastoma gene product, pRb, which was prevented by activated ras. Apoptosis and pRb hypophosphorylation were associated with a reduction in cyclin D1 levels, suggesting that the growth-retarding effects of TPA were produced by modulation of this cell cycle protein. Interestingly, the mechanism of protection by activated ras did not seem to result from downstream activation of phosphatidylinositol-3-kinase (PI3K) as has been implicated in other systems. Additional analysis revealed that TPA-induced apoptosis was associated with the downregulation of the anti-apoptotic proteins Bcl-x and Mcl-1 and dependent on the activity of the transcription factor Jun.

journal_name

Arch Biochem Biophys

journal_title

Archives of biochemistry and biophysics

authors

Lee RG,Rosson D

doi

10.1006/abbi.2000.2182

subject

Has Abstract

pub_date

2001-01-15 00:00:00

pages

378-86

issue

2

eissn

0003-9861

issn

1096-0384

pii

S0003986100921829

journal_volume

385

pub_type

杂志文章

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