Phosphatidylinositol-3 kinase is necessary for 12-O-tetradecanoylphorbol 13-acetate-induced cell transformation and activated protein 1 activation

Huang, Chuanshu; Schmid, Patricia C.; Ma, Wei-Ya; Schmid, HaraldH.O.; Dong, Zigang

doi:10.1074/jbc.272.7.4187

Cited by 109Protein Kinase Regulation and GTPase SignalingPI3K/AKT/mTOR signaling in cancerSignaling Pathways in Disease

Phosphatidylinositol-3 kinase is necessary for 12-O-tetradecanoylphorbol 13-acetate-induced cell transformation and activated protein 1 activation

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Huang, Chuanshu, Schmid, Patricia C., Ma, Wei-Ya, Schmid, HaraldH.O., Dong, Zigang·1997·Journal of Biological Chemistry

DOI 10.1074/jbc.272.7.4187

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Abstract

Phorbol esters, which activate isoforms of protein kinase C, are general activators of the transcription factor activated protein 1 (AP-1). The pathway involved in this signal transduction is not very clear. Currently, little is known about whether phosphatidylinositol-3 (PI-3) kinase plays any role in phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced signal transduction. We demonstrate here that TPA not only has markedly synergistic effects on insulin-induced PI-3 kinase activity, but it also can induce PI-3 kinase activity and the PI-3 phosphates by itself. We also found that insulin, a PI-3 kinase activator, enhanced TPA-induced AP-1 trans-activation and transformation in JB6 promotion-sensitive cells. Furthermore, wortmannin and LY294002, two PI-3 kinase inhibitors, markedly decreased AP-1 activity induced by insulin, TPA, or TPA and insulin and inhibited JB6 promotion-sensitive cell transformation induced by TPA or TPA and insulin. Most importantly, constitutive overexpression of the dominant negative PI-3 kinase P85 mutants completely blocked insulin- or TPA-induced AP-1 trans-activation and TPA-induced cell transformation. All evidence from present studies suggests that PI-3 kinase acts as a mediator in TPA-induced AP-1 activation and transformation in JB6 cells.

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“Additionally, along with ROS's known direct stimulation of MMPs, AP-1 is also known to induce MMPs in human skin that, in turn, activates collagen degradation [2,103].”
From Equol’s Anti-Aging Effects Protect against Environmental Assaults by Increasing Skin Antioxidant Defense and ECM Proteins While Decreasing Oxidative Stress and Inflammation (2018) · cites this paper as [103]
AP-1-induced MMPs activate collagen degradation.
“Additionally, along with ROS's known direct stimulation of MMPs, AP-1 is also known to induce MMPs in human skin that, in turn, activates collagen degradation [2,103].”
From Equol’s Anti-Aging Effects Protect against Environmental Assaults by Increasing Skin Antioxidant Defense and ECM Proteins While Decreasing Oxidative Stress and Inflammation (2018) · cites this paper as [103]
ROS directly stimulates MMPs.
“Additionally, along with ROS's known direct stimulation of MMPs, AP-1 is also known to induce MMPs in human skin that, in turn, activates collagen degradation [2,103].”
From Equol’s Anti-Aging Effects Protect against Environmental Assaults by Increasing Skin Antioxidant Defense and ECM Proteins While Decreasing Oxidative Stress and Inflammation (2018) · cites this paper as [103]

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Authors: Huang, C., Schmid, P. C., Ma, W.-Y., Schmid, H. O., & Dong, Z.
Affiliations: University of Minnesota (US)
Corresponding author: Dong, Zigang
ORCID: Huang, Chuanshu
Dong, Zigang
Venue: Journal of Biological Chemistry
Publisher: Elsevier BV
Published: 1997-02
Volume: 272
Issue: 7
Pages: 4187-4194
ISSN: 0021-9258 (ISSN-L)
DOI: 10.1074/jbc.272.7.4187
OpenAlex: W2069148122
Cited by: 109
References: 54
Citations by year: 2018: 1 · 2016: 2 · 2015: 2 · 2013: 1 · 2012: 3
FWCI: 2.61
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
creativecommons.org/licenses/by/4.0/ (vor, 8650 d)
Locations: Journal of Biological Chemistry (publishedVersion, cc-by)
PubMed (publishedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
Keywords: phosphatidylinositol 3-kinase, phorbol myristate acetate, phorbol ester, cell transformation, insulin signaling, signal transduction, wortmannin, LY294002, JB6 cells, protein kinase C
MeSH terms: Wortmannin, Epidermal Cells, Androstadienes, Animals, Cell Line, Cell Transformation, Neoplastic, Chromones, Drug Interactions, Enzyme Activation, Enzyme Inhibitors, Epidermis, Insulin, Morpholines, Tetradecanoylphorbol Acetate, Phosphotransferases (Alcohol Group Acceptor), Transcription Factor AP-1, Phosphatidylinositol 3-Kinases, Mice

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Phosphatidylinositol-3 kinase is necessary for 12-O-tetradecanoylphorbol 13-acetate-induced cell transformation and activated protein 1 activation

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