Role of Class II Nuclear Receptors in Liver Carcinogenesis

被引:8
作者
Li, Guodong [1 ,2 ]
Guo, Grace L. [1 ]
机构
[1] Univ Kansas, Med Ctr, Dept Pharmacol Toxicol & Therapeut, Kansas City, KS 66160 USA
[2] Harbin Med Univ, Canc Treatment Ctr, Dept Abdominal Surg, Affiliated Hosp 4, Harbin, Peoples R China
关键词
Class II nuclear receptors; constitutive androstane receptor; farnesoid X receptor; hepatocellular carcinoma; liver X receptors; pregnane X receptor; peroxisome proliferator-activated receptors; retinoic acid receptors; PROLIFERATOR-ACTIVATED RECEPTORS; RETINOIC-ACID-RECEPTOR; CONSTITUTIVE ACTIVE/ANDROSTANE RECEPTOR; PREGNANE-X-RECEPTOR; UNION-OF-PHARMACOLOGY; BETA/DELTA PPAR-BETA/DELTA; GLOBAL CANCER STATISTICS; E-2 SIGNALING PATHWAYS; CELL-CYCLE ARREST; HEPATOCELLULAR-CARCINOMA;
D O I
10.2174/187152011796011064
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Nuclear receptors (NRs) are ligand-activated transcription factors that are important to life by regulating a wide variety of physiological and pathological functions. There are three classes of NRs defined by ligands and heterodimer partners. The Class II NRs are involved in a broad range of pathophysiological functions in the liver, including cholesterol and bile acid homeostasis; lipid and glucose metabolism; inflammation; liver regeneration and hepatocellular carcinogenesis. Due to highly complicated molecular mechanisms in the development and progression of hepatocellular carcinoma (HCC), HCC is still one of the most common malignancies in the world. Given the pivotal functions of the Class II NRs in the liver, the roles of these NRs in hepatocellular carcinogenesis are emerging. This review summarizes the roles of Class II NRs in liver carcinogenesis and their potential application in the prevention and treatment of HCC.
引用
收藏
页码:529 / 542
页数:14
相关论文
共 247 条
[1]   Steroid hormone receptors in cancer development A target for cancer therapeutics [J].
Ahmad, Nihal ;
Kumar, Raj .
CANCER LETTERS, 2011, 300 (01) :1-9
[2]   Issues and updates: evaluating estrogen receptor-α, progesterone receptor, and HER2 in breast cancer [J].
Allred, D. Craig .
MODERN PATHOLOGY, 2010, 23 :S52-S59
[3]   Trim24 targets endogenous p53 for degradation [J].
Allton, Kendra ;
Jain, Abhinav K. ;
Herz, Hans-Martin ;
Tsai, Wen-Wei ;
Jung, Sung Yun ;
Qin, Jun ;
Bergmann, Andreas ;
Johnson, Randy L. ;
Barton, Michelle Craig .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2009, 106 (28) :11612-11616
[4]  
[Anonymous], 2009, CANCER BIOL THER
[5]   Molecular Mechanisms of Hepatocellular Carcinoma [J].
Aravalli, Rajagopal N. ;
Steer, Clifford J. ;
Cressman, Erik N. K. .
HEPATOLOGY, 2008, 48 (06) :2047-2063
[6]   Tissue distribution and quantification of the expression of mRNAs of peroxisome proliferator-activated receptors and liver X receptor-alpha in humans - No alteration in adipose tissue of obese and NIDDM patients [J].
Auboeuf, D ;
Rieusset, J ;
Fajas, L ;
Vallier, P ;
Frering, V ;
Riou, JP ;
Staels, P ;
Auwerx, J ;
Laville, M ;
Vidal, H .
DIABETES, 1997, 46 (08) :1319-1327
[7]  
Auwerx J, 1999, CELL, V97, P161
[8]   A NEW ORPHAN MEMBER OF THE NUCLEAR HORMONE-RECEPTOR SUPERFAMILY THAT INTERACTS WITH A SUBSET OF RETINOIC ACID RESPONSE ELEMENTS [J].
BAES, M ;
GULICK, T ;
CHOI, HS ;
MARTINOLI, MG ;
SIMHA, D ;
MOORE, DD .
MOLECULAR AND CELLULAR BIOLOGY, 1994, 14 (03) :1544-1552
[9]   A nuclear receptor atlas: Macrophage activation [J].
Barish, GD ;
Downes, M ;
Alaynick, WA ;
Yu, RT ;
Ocampo, CB ;
Bookout, AL ;
Mangelsdorf, DJ ;
Evans, RM .
MOLECULAR ENDOCRINOLOGY, 2005, 19 (10) :2466-2477
[10]  
Bauer B, 2004, MOL PHARMACOL, V66, P413