Book contents
- Frontmatter
- Dedication
- Contents
- List of Contributors
- Preface
- Part 1.1 Analytical techniques: analysis of DNA
- Part 1.2 Analytical techniques: analysis of RNA
- Part 2.1 Molecular pathways underlying carcinogenesis: signal transduction
- Part 2.2 Molecular pathways underlying carcinogenesis: apoptosis
- Part 2.3 Molecular pathways underlying carcinogenesis: nuclear receptors
- 32 Androgens and the androgen receptor (AR)
- 33 Emerging roles of peroxisome proliferator-activated receptor gamma in cancer
- Part 2.4 Molecular pathways underlying carcinogenesis: DNA repair
- Part 2.5 Molecular pathways underlying carcinogenesis: cell cycle
- Part 2.6 Molecular pathways underlying carcinogenesis: other pathways
- Part 3.1 Molecular pathology: carcinomas
- Part 3.2 Molecular pathology: cancers of the nervous system
- Part 3.3 Molecular pathology: cancers of the skin
- Part 3.4 Molecular pathology: endocrine cancers
- Part 3.5 Molecular pathology: adult sarcomas
- Part 3.6 Molecular pathology: lymphoma and leukemia
- Part 3.7 Molecular pathology: pediatric solid tumors
- Part 4 Pharmacologic targeting of oncogenic pathways
- Index
- References
33 - Emerging roles of peroxisome proliferator-activated receptor gamma in cancer
from Part 2.3 - Molecular pathways underlying carcinogenesis: nuclear receptors
Published online by Cambridge University Press: 05 February 2015
- Frontmatter
- Dedication
- Contents
- List of Contributors
- Preface
- Part 1.1 Analytical techniques: analysis of DNA
- Part 1.2 Analytical techniques: analysis of RNA
- Part 2.1 Molecular pathways underlying carcinogenesis: signal transduction
- Part 2.2 Molecular pathways underlying carcinogenesis: apoptosis
- Part 2.3 Molecular pathways underlying carcinogenesis: nuclear receptors
- 32 Androgens and the androgen receptor (AR)
- 33 Emerging roles of peroxisome proliferator-activated receptor gamma in cancer
- Part 2.4 Molecular pathways underlying carcinogenesis: DNA repair
- Part 2.5 Molecular pathways underlying carcinogenesis: cell cycle
- Part 2.6 Molecular pathways underlying carcinogenesis: other pathways
- Part 3.1 Molecular pathology: carcinomas
- Part 3.2 Molecular pathology: cancers of the nervous system
- Part 3.3 Molecular pathology: cancers of the skin
- Part 3.4 Molecular pathology: endocrine cancers
- Part 3.5 Molecular pathology: adult sarcomas
- Part 3.6 Molecular pathology: lymphoma and leukemia
- Part 3.7 Molecular pathology: pediatric solid tumors
- Part 4 Pharmacologic targeting of oncogenic pathways
- Index
- References
Summary
Focus
The peroxisome proliferator-activated receptors (PPARs) are ligand-activated nuclear receptors, which include PPARα, PPARγ, and PPARδ (1). PPARγ was initially cloned as a transcription factor involved in adipocyte differentiation. Subsequent studies suggested a broad spectrum of PPARγ functions in lipid metabolism, inflammation, atherogenesis, and cell differentiation, as well as in tumorigenesis. Herein, we review recent studies suggesting a dominant role for PPARγ in processes related to cancer initiation and progression, and describe the mechanisms by which PPARγ regulates cell-cycle progression, cell death, and angiogenesis.
Structural features of PPARγ
There are three PPARγ isoforms (γ1, γ2, and γ3). Both PPARγ1 and PPARγ2 are abundantly expressed in adipose tissue, whereas PPARγ1 expression is detected in liver, spleen, heart tissues, and epithelium of a variety of tissues including breast and prostate. Their modular structure resembles other nuclear hormone receptors with an N-terminal activation function 1 (AF-1), a DNA-binding domain (DBD), and a C-terminal ligand-binding domain (activation function 2, AF-2).
- Type
- Chapter
- Information
- Molecular OncologyCauses of Cancer and Targets for Treatment, pp. 392 - 402Publisher: Cambridge University PressPrint publication year: 2013