Effects of the CDK-inhibitor CYC202 on p38 MAPK, ERK1/2 and c-Myc activities in papillomavirus type 16 E6- and E7-transformed human keratinocytes

Ganka Atanasova, Antonia R. Isaeva, Nikolai Zhelev, Yves Poumay, Vanyo I. Mitev

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Abstract

In the present study, we have investigated the effect of the chemical CDK-inhibitor CYC202 on E6 and E7-transformed keratinocytes, in which the function of the cellular cell cycle inhibitor p21Cip1 is abrogated by the viral genes. The cyto-toxicity and the inhibition of the cell growth were analysed by MTT assay and analysis of DNA synthesis respectively. The effect on some signalling molecules was tested by Western blot analysis. CYC202 effectively inhibited the proliferation of E6 and E7 keratinocytes in a dose-dependent manner. Treatment with CYC202 strongly increased the activity of p38 MAP kinase. Furthermore, it inhibited ERK1/2 at the highest concentration used and had no effect on the activity of JNK1/2. CYC202 also increased the phosphorylation of HSP27 and decreased the phosphorylation and DNA-binding activity of the transcriptional regulator c-Myc, in correlation with the corresponding upstream kinases p38 MAPK and ERK1/2. Our results provide additional data for the anti-proliferative actions and potency of the chemical CDK-inhibitor CYC202.
Original languageEnglish
Pages (from-to)999-1005
Number of pages7
JournalOncology Reports
Volume18
Issue number4
StatePublished - Oct 2007

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p38 Mitogen-Activated Protein Kinases
Keratinocytes
Phosphorylation
DNA
Mitogen-Activated Protein Kinase 3
Viral Genes
Cell Cycle
Western Blotting

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Atanasova, Ganka; Isaeva, Antonia R.; Zhelev, Nikolai; Poumay, Yves; Mitev, Vanyo I. / Effects of the CDK-inhibitor CYC202 on p38 MAPK, ERK1/2 and c-Myc activities in papillomavirus type 16 E6- and E7-transformed human keratinocytes.

In: Oncology Reports, Vol. 18, No. 4, 10.2007, p. 999-1005.

Research output: Contribution to journalArticle

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title = "Effects of the CDK-inhibitor CYC202 on p38 MAPK, ERK1/2 and c-Myc activities in papillomavirus type 16 E6- and E7-transformed human keratinocytes",
abstract = "In the present study, we have investigated the effect of the chemical CDK-inhibitor CYC202 on E6 and E7-transformed keratinocytes, in which the function of the cellular cell cycle inhibitor p21Cip1 is abrogated by the viral genes. The cyto-toxicity and the inhibition of the cell growth were analysed by MTT assay and analysis of DNA synthesis respectively. The effect on some signalling molecules was tested by Western blot analysis. CYC202 effectively inhibited the proliferation of E6 and E7 keratinocytes in a dose-dependent manner. Treatment with CYC202 strongly increased the activity of p38 MAP kinase. Furthermore, it inhibited ERK1/2 at the highest concentration used and had no effect on the activity of JNK1/2. CYC202 also increased the phosphorylation of HSP27 and decreased the phosphorylation and DNA-binding activity of the transcriptional regulator c-Myc, in correlation with the corresponding upstream kinases p38 MAPK and ERK1/2. Our results provide additional data for the anti-proliferative actions and potency of the chemical CDK-inhibitor CYC202.",
author = "Ganka Atanasova and Isaeva, {Antonia R.} and Nikolai Zhelev and Yves Poumay and Mitev, {Vanyo I.}",
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Effects of the CDK-inhibitor CYC202 on p38 MAPK, ERK1/2 and c-Myc activities in papillomavirus type 16 E6- and E7-transformed human keratinocytes. / Atanasova, Ganka; Isaeva, Antonia R.; Zhelev, Nikolai; Poumay, Yves; Mitev, Vanyo I.

In: Oncology Reports, Vol. 18, No. 4, 10.2007, p. 999-1005.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Effects of the CDK-inhibitor CYC202 on p38 MAPK, ERK1/2 and c-Myc activities in papillomavirus type 16 E6- and E7-transformed human keratinocytes

AU - Atanasova,Ganka

AU - Isaeva,Antonia R.

AU - Zhelev,Nikolai

AU - Poumay,Yves

AU - Mitev,Vanyo I.

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AB - In the present study, we have investigated the effect of the chemical CDK-inhibitor CYC202 on E6 and E7-transformed keratinocytes, in which the function of the cellular cell cycle inhibitor p21Cip1 is abrogated by the viral genes. The cyto-toxicity and the inhibition of the cell growth were analysed by MTT assay and analysis of DNA synthesis respectively. The effect on some signalling molecules was tested by Western blot analysis. CYC202 effectively inhibited the proliferation of E6 and E7 keratinocytes in a dose-dependent manner. Treatment with CYC202 strongly increased the activity of p38 MAP kinase. Furthermore, it inhibited ERK1/2 at the highest concentration used and had no effect on the activity of JNK1/2. CYC202 also increased the phosphorylation of HSP27 and decreased the phosphorylation and DNA-binding activity of the transcriptional regulator c-Myc, in correlation with the corresponding upstream kinases p38 MAPK and ERK1/2. Our results provide additional data for the anti-proliferative actions and potency of the chemical CDK-inhibitor CYC202.

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JF - Oncology Reports

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