Interactions between Myc and Mediators of Inflammation in Chronic Liver Diseases

被引：60
作者：
Liu, Ting [1 ]
Zhou, Yu [2 ]
Ko, Kwang Suk [3 ]
Yang, Heping [4 ]
机构：
[1] Cent S Univ, Xiangya Hosp, Dept Gastroenterol, Changsha 410008, Hunan, Peoples R China
[2] Univ So Calif, Keck Sch Med, GI Liver Ctr, Los Angeles, CA 90033 USA
[3] Ewha Womans Univ, Coll Hlth Sci, Dept Nutr Sci & Food Management, Seoul 150750, South Korea
[4] Cedars Sinai Med Ctr, Dept Med, Div Gastroenterol, Los Angeles, CA 90048 USA
来源：
MEDIATORS OF INFLAMMATION | 2015年 / 2015卷
基金：
中国国家自然科学基金;
关键词：
NF-KAPPA-B; TUMOR-NECROSIS-FACTOR; HEPATIC STELLATE CELLS; C-MYC; FATTY LIVER; SOLUBLE INTERLEUKIN-2-RECEPTOR; TRANSCRIPTION FACTORS; RECEPTOR ANTAGONIST; BILIARY-CIRRHOSIS; IL-8; EXPRESSION;
D O I：
10.1155/2015/276850
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Most chronic liver diseases (CLDs) are characterized by inflammatory processes with aberrant expressions of various pro-and anti-inflammatory mediators in the liver. These mediators are the driving force of many inflammatory liver disorders, which often result in fibrosis, cirrhosis, and liver tumorigenesis. c-Myc is involved in many cellular events such as cell growth, proliferation, and differentiation. c-Myc upregulates IL-8, IL-10, TNF-alpha, and TGF-beta, while IL-1, IL-2, IL-4, TNF-alpha, and TGF-beta promote c-Myc expression. Their interactions play a central role in fibrosis, cirrhosis, and liver cancer. Molecular interference of their interactions offers possible therapeutic potential for CLDs. In this review, current knowledge of the molecular interactions between c-Myc and various well known inflammatory mediators is discussed.
引用
收藏
页数：12
相关论文
共 139 条
  • [1] Akiba J, 2001, INT J ONCOL, V18, P257
  • [2] Ali Mohamed A, 2004, Egypt J Immunol, V11, P83
  • [3] Synergy between truncated c-Met (cyto-Met) and c-Myc in liver oncogenesis:: Importance of TGF-β signalling in the control of liver homeostasis and transformation
    Amicone, L
    Terradillos, O
    Calvo, L
    Costabile, B
    Cicchini, C
    Della Rocca, C
    Lozupone, F
    Piacentini, M
    Buendia, MA
    Tripodi, M
    [J]. ONCOGENE, 2002, 21 (09) : 1335 - 1345
  • [4] [Anonymous], MOL CELLULAR BIOL
  • [5] [Anonymous], EVID BASED COMPLEMEN
  • [6] Is interleukin-1 a good or bad 'guy' in tumor immunobiology and immunotherapy?
    Apte, Ron N.
    Voronov, Elena
    [J]. IMMUNOLOGICAL REVIEWS, 2008, 222 : 222 - 241
  • [7] Helicobacter pylori Induces ERK-dependent Formation of a Phospho-c-Fos.c-Jun Activator Protein-1 Complex That Causes Apoptosis in Macrophages
    Asim, Mohammad
    Chaturvedi, Rupesh
    Hoge, Svea
    Lewis, Nuruddeen D.
    Singh, Kshipra
    Barry, Daniel P.
    Algood, Holly S.
    de Sablet, Thibaut
    Gobert, Alain P.
    Wilson, Keith T.
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2010, 285 (26) : 20343 - 20357
  • [8] c-Myc regulates cell size and ploidy but is not essential for postnatal proliferation in liver
    Baena, E
    Gandarillas, A
    Vallespinós, M
    Zanet, J
    Bachs, O
    Redondo, C
    Fabregat, I
    Martinez, C
    de Alborán, IM
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2005, 102 (20) : 7286 - 7291
  • [9] Drug-Induced Liver Injury due to Cancer Chemotherapeutic Agents
    Bahirwani, Ranjeeta
    Reddy, K. Rajender
    [J]. SEMINARS IN LIVER DISEASE, 2014, 34 (02) : 162 - 171
  • [10] c-Myc is essential for vasculogenesis and angiogenesis during development and tumor progression
    Baudino, TA
    McKay, C
    Pendeville-Samain, H
    Nilsson, JA
    Maclean, KH
    White, EL
    Davis, AC
    Ihle, JN
    Cleveland, JL
    [J]. GENES & DEVELOPMENT, 2002, 16 (19) : 2530 - 2543
12345678910