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Constitutive expression of human keratin 14 gene in mouse lung induces premalignant lesions and squamous differentiation

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  • Squamous Cell Carcinoma Accounts For 20% Of All Human Lung Cancers And Is Strongly Linked To Cigaret
  • It Develops Through Premalignant Changes That Are Characterized By High Levels Of Keratin 14 (K14) E
  • Squamous Metaplasia And Dysplasia To Carcinoma In Situ And Invasive Carcinoma
  • In Order To Explore The Impact Of K14 In The Pulmonary Epithelium That Normally Lacks Both Squamous
  • Human Keratin 14 Gene Hk14 Was Constitutively Expressed In Mouse Airway Progenitor Cells Using A Mou
  • While The Lungs Of Cc10-Hk14 Transgenic Mice Developed Normally
  • We Detected Increased Expression Of K14 And The Molecular Markers Of Squamous Differentiation Progra
  • Loricrin
  • Small Proline-Rich Protein 1A
  • Transglutaminase 1 And Cholesterol Sulfotransferase 2B1
  • In Contrast
  • Wild-Type Lungs Were Negative
  • Aging Cc10-Hk14 Mice Revealed Multifocal Airway Cell Hyperplasia
  • Occasional Squamous Metaplasia And Their Lung Tumors Displayed Evidence For Multidirectional Differe
  • We Conclude That Constitutive Expression Of Hk14 Initiates Squamous Differentiation Program In The M
  • But Fails To Promote Squamous Maturation
  • Our Study Provides A Novel Model For Assessing The Mechanisms Of Premalignant Lesions In Vivo By Mod
  • © The Author 2008
  • Published By Oxford University Press
  • All Rights Reserved
  • Biology


Chapter 2 Androgen Action During Prostate Carcinogenesis Diping Wang and Donald J. Tindall Abstract Androgens are critical for normal prostate development and function, as well as prostate cancer initiation and progression. Androgens function mainly by regulating target gene expression through the androgen receptor (AR). Many studies have shown that androgen-AR signaling exerts actions on key events during prostate carcinogenesis. In this review, androgen action in distinct aspects of prostate carcinogenesis, including (i) cell proliferation, (ii) cell apoptosis, and (iii) prostate cancer metastasis will be discussed. Key words: Androgen receptor, prostate cancer, androgen metabolism, androgen signaling, castration-resistant prostate cancer. 1. Androgen Signaling Androgens are the male sex hormones, which control the differ- entiation and maturation of male reproductive organs, including the prostate gland. Testosterone is the principal androgen in cir- culation and is synthesized by Leydig cells in the testes, under the regulation of luteinizing hormone (LH), which is further regulated by gonadotropin-releasing hormone (GnRH). Adrenal glands also synthesize a small amount of androgens, such as dehy- droepiandrosterone (DHEA) and androstenedione (4-dione) (1). Testosterone enters prostate cells by passive diffusion, where it is converted enzymatically by 5-α reductases to the more potent androgen dihydrotestosterone (DHT) (2). Binding of androgens to the androgen receptor (AR), a ligand-modulated transcrip- tion factor, induces a conformational change in the AR, causing release of heat shock proteins and translocation of the AR to the F. Saatcioglu (ed.), Androgen Action, Methods in Molecular Biology 776, DOI 10.1007/978-1-61779-243-4_2, © Springer Science+Business Media, LLC 2011 25 26 Wang and Tindall nucleus, where it transcriptionally regulates the expression of tar- get genes (3). In addition to the classic genomic effects of sex steroids, accu- mulating

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