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Chromatin and cancer: Causes and consequences
Author(s) -
Singh Harpreet,
Sekinger Edward A.,
Gross David S.
Publication year - 2000
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/1097-4644(2000)79:35+<61::aid-jcb1127>3.0.co;2-z
Subject(s) - chromatin , biology , bivalent chromatin , microbiology and biotechnology , chromatin remodeling , promoter , chia pet , transcription factor , gene , genetics , gene expression
In this review, we discuss recent evidence implicating chromatin structure in the etiology of cancer. In particular, we present evidence indicating that inappropriate regulation of chromatin structure inhibits normal cell differentiation pathways and stimulates uncontrolled cell proliferation, with the outcome being oncogenesis. Such inappropriate chromatin structures arise as a consequence of (i) chromosomal rearrangements that fuse gene‐specific activators with global co‐regulators, drastically altering activator function; (ii) hypermethylation of tumor suppressor gene promoters, resulting in their inactivation; or (iii) mistargeted nuclear compartmentalization of growth‐control genes and their regulators, resulting in the up‐ or down‐regulation of such genes. How does chromatin silence genes? Recent results from model in vivo systems argues that chromatin can repress transcription at two levels: (i) by sterically interfering with the binding of transcription factors to the promoter, thereby blocking initiation; and (ii) at a step subsequent to the binding of activators and recruitment of the preinitiation complex. J. Cell. Biochem. Suppl. 35:61–68, 2000. © 2001 Wiley‐Liss, Inc.