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Peroxisome proliferator‐activated receptor gamma coactivator‐1 alpha (PGC‐1α) upregulated E‐cadherin expression in HepG2 cells
Author(s) -
Lee Hui-Ju,
Su Yeu,
Lui Wing-Yiu,
Chau Gar-Yang,
Yin Pen-Hui,
Lee Hsin-Chen,
Chi Chin-Wen
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.01.033
Subject(s) - coactivator , transactivation , chromatin immunoprecipitation , downregulation and upregulation , peroxisome proliferator activated receptor , nuclear receptor , nuclear receptor coactivator 1 , transfection , peroxisome proliferator activated receptor alpha , chemistry , microbiology and biotechnology , biology , receptor , transcription factor , gene expression , biochemistry , promoter , gene
Peroxisome proliferator‐activated receptor gamma coactivator‐1 alpha (PGC‐1α), a highly inducible transcriptional coactivator regulating energy homeostasis, is down‐regulated in hepatoma tissues. To dissect its role in hepato‐tumorigenesis, Ingenuity ® Pathway Analysis was applied to construct pathways affected by PGC‐1α upregulation in HepG2 hepatoma cells based on our microarray data. Interestingly, migration of these cells was markedly diminished by PGC‐1α overexpression in consistency with Ingenuity ® results. Moreover, a deduced expression increase of E‐cadherin was also observed in PGC‐1α‐overexpressing HepG2 cells. Finally, transient transfection and chromatin‐immunoprecipitation assays suggested that increased histone acetylation might be responsible for PGC‐1α‐mediated transactivation of a minimal E‐cadherin promoter.