Abstract
The ARF tumor suppressor gene antagonizes generation of various tumors. ARF-mediated tumor suppression occurs in a p53-independent manner as well as in a p53-dependent manner. We here demonstrate that BCL6 is a target of the ARF tumor suppressor. Either mouse p19(ARF) or human p14(ARF) binds to BCL6 and downregulates BCL6-induced transcriptional repression. ARF-mediated downregulation of the BCL6 activity may account in part for ARF-mediated tumor suppression.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Binding Sites
-
COS Cells
-
Cell Line
-
Chlorocebus aethiops
-
Cyclin-Dependent Kinase Inhibitor p16
-
DNA-Binding Proteins / metabolism*
-
Down-Regulation*
-
Humans
-
Mice
-
Osteosarcoma / metabolism*
-
Protein Binding
-
Protein Structure, Tertiary
-
Proto-Oncogene Proteins / metabolism*
-
Proto-Oncogene Proteins c-bcl-6
-
Transcription Factors / metabolism*
-
Transcriptional Activation*
-
Tumor Suppressor Protein p14ARF / metabolism*
-
Tumor Suppressor Proteins / metabolism*
Substances
-
Cdkn2a protein, mouse
-
Cyclin-Dependent Kinase Inhibitor p16
-
DNA-Binding Proteins
-
Proto-Oncogene Proteins
-
Proto-Oncogene Proteins c-bcl-6
-
Transcription Factors
-
Tumor Suppressor Protein p14ARF
-
Tumor Suppressor Proteins