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1

The expression of protein kinase B in gastric cancer cell apoptosis induced 12-O-tetradecanoylphorbol-1,3-acetate

100%
Zhang B., Xia C.
Cellular and Molecular Biology Letters
|
2009
|
tom 14
|
nr 3
466-480
Protein kinase B (PKB/Akt) is a serine-threonine kinase functioning downstream of phosphatidylinositol 3-kinase (PI-3 kinase) in response to mitogen or growth factor stimulation. In several cell types, it plays an important anti-apoptotic role. TPA is a potent regulator of the growth of many different cell types. Here, we detected that TPA could induce cell apoptosis in the gastric cancer cell line, BGC-823. We also found that TPA inhibited the expression of PKB/Akt in a TPA concentration- and time-dependent manner. Furthermore, TPA inhibited the phosphorylation of PKB at Ser473, but did not affect the phosphorylation of Thr308. It only attenuated the expression of PKB/Akt and the phosphorylation of Ser473 in the cell nucleus, whereas it did not change the PKB/Akt distribution in BGC-823 cells. These results suggest that PKB/Akt inhibition by TPA may be the important factor in the mechanism of effect of TPA on gastric cell lines.
2

12-O-tetradecanoylphorbol-1,3-acetate induces the negative regulation of protein kinase B by protein kinase Calpha during gastric cancer cell apoptosis

100%
Zhang B., Xia C.
Cellular and Molecular Biology Letters
|
2010
|
tom 15
|
nr 3
377-394
The PKB signaling pathway is essential for cell survival and the inhibition of apoptosis, but its functional mechanisms have not been fully explored. Previously, we reported that TPA effectively inhibited PKB activity and caused PKB degradation, which was correlated with the repression of PKB phosphorylation at Ser473. In this study, we focus on how PKB is regulated by TPA in gastric cancer cells. One of the TPA targets, PKCα, was found to mediate the inhibition of PKB phosphorylation and degredation caused by TPA. Furthermore, TPA induced the import of PKCα into the nucleus, where PKCα exerted an inhibitory effect on PKB expression and phosphorylation. As a result, cancer cell proliferation was arrested. Our study characterizes a novel function of PKCα in mediating the negative regulation of PKB by TPA, and suggests a potential application in the clinical treatment of gastric cancer.
3
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Effects of naturally occurring plant phenols on production of reactive oxygen species and DNA damage induced by tumour promoter 12-O-tetradecanoyl phorbol-13-acetate (TPA) in mouse epidermis

84%
Ignatowicz E., Zielinska-Przyjemska M., Szaefer H., Sobierajska H., Baer-Dubowska W.
Herba Polonica
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2012
|
tom 58
|
nr 4
Naturally occurring phenolics: protocatechuic, chlorogenic, tannic acids and trihydroxystilbene and resveratrol were shown to inhibit multistage carcinogenesis in animal models, including mouse epidermis. Treatment of mouse skin with tumor promoter 12-Otetradecanoyl phorbol-13-acetate (TPA) may induce ROS production in keratinocytes and skin infiltrating leukocytes. In our study, the effect of these phenolics on intracellular ROS production and DNA damage was examined. ROS were analysed by flow cytometry, while DNA damage by comet assay. Following treatment with TPA (6.8 nmol/mouse) two subpopulations of epidermal cells were identified. Pretreatment of mice with 16 mmol of phenolics decreased ROS production in both subpopulations. The most efficient inhibitors of ROS in whole population of keratinocytes were chlorogenic acid and resveratrol. Tannic acid reduced the most DNA damage induced by TPA treatment. These results suggest that anti-promotional effects of these two plant phenols might be partially explained by the inhibition of TPA-induced inflammation.
4

12-O-tetradecanoylphorbol-1,3-acetate-induced degradation of protein kinase B via ubiquitin-proteasomal pathway depends on its Ser473 phosphorylation in gastric cancer cells

67%
Zhang B., Xia C.
Folia Histochemica et Cytobiologica
|
2013
|
tom 51
|
nr 1
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