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Link to original content: https://pubmed.ncbi.nlm.nih.gov/16230382
Regulation of Kruppel-like factor 6 tumor suppressor activity by acetylation - PubMed Skip to main page content
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. 2005 Oct 15;65(20):9216-25.
doi: 10.1158/0008-5472.CAN-05-1040.

Regulation of Kruppel-like factor 6 tumor suppressor activity by acetylation

Dan Li  1 , Steven Yea, Georgia Dolios, John A Martignetti, Goutham Narla, Rong Wang, Martin J Walsh, Scott L Friedman
Affiliations

Regulation of Kruppel-like factor 6 tumor suppressor activity by acetylation

Dan Li et al. Cancer Res. .

Abstract

Krüppel-like factor 6 (KLF6) is a zinc finger transcription factor and tumor suppressor that is inactivated in a number of human cancers by mutation, allelic loss, and/or promoter methylation. A key mechanism of growth inhibition by wild-type KLF6 is through p53-independent up-regulation of p21(WAF1/cip1) (CDKN1A), which is abrogated in several tumor-derived mutants. Here we show by chromatin immunoprecipitation that transactivation of p21(WAF1/cip1) by KLF6 occurs through its direct recruitment to the p21(WAF1/cip1) promoter and requires acetylation by histone acetyltransferase activity of either cyclic AMP-responsive element binding protein-binding protein or p300/CBP-associated factor. Direct lysine acetylation of KLF6 peptides can be shown by mass spectrometry. A single lysine-to-arginine point mutation (K209R) derived from prostate cancer reduces acetylation of KLF6 and abrogates its capacity to up-regulate endogenous p21(WAF1/cip1) and reduce cell proliferation. These data indicate that acetylation may regulate KLF6 function, and its loss in some tumor-derived mutants could contribute to its failure to suppress growth in prostate cancer.

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