Expression and Function of Kruppel Like-Factors (KLF) in Carcinogenesis
Krüppel-like factor (KLF) family members share a three C2H2 zinc finger DNA binding domain, and are involved in cell proliferation and differentiation control in normal as in pathological situations. Studies over the past several years support a significant role for this family of transcription fact...
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2009
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pubmed-27299992010-02-01 Expression and Function of Kruppel Like-Factors (KLF) in Carcinogenesis Bureau, Christophe Hanoun, Naima Torrisani, Jérôme Vinel, Jean-Pierre Buscail, Louis Cordelier, Pierre Article Krüppel-like factor (KLF) family members share a three C2H2 zinc finger DNA binding domain, and are involved in cell proliferation and differentiation control in normal as in pathological situations. Studies over the past several years support a significant role for this family of transcription factors in carcinogenesis. KLFs can both activate and repress genes that participate in cell-cycle regulation. Among them, many up-regulated genes are inhibitors of proliferation, whereas genes that promote cell proliferation are repressed. However, several studies do present KLFs as positive regulator of cell proliferation. KLFs can be deregulated in multiple cancers either by loss of heterozygosity (LOH), somatic mutation or transcriptional silencing by promoter hypermethylation. Accordingly, KLF expression was shown to mediate growth inhibition when ectopically expressed in multiple cancer-derived cell lines through the inhibition of a number of key oncogenic signaling pathways, and to revert the tumorogenic phenotype in vivo. Taken together, these observations suggest that KLFs act as tumor suppressor. However, in some occasion, KLFs could act as tumor promoters, depending on “cellular context”. Thus, this review will discuss the roles and the functions of KLF family members in carcinogenesis, with a special focus on cancers from epithelial origin. Bentham Science Publishers Ltd. 2009-08 /pmc/articles/PMC2729999/ /pubmed/20119532 http://dx.doi.org/10.2174/138920209788921010 Text en ©2009 Bentham Science Publishers Ltd. http://creativecommons.org/licenses/by/2.5/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.5/), which permits unrestrictive use, distribution, and reproduction in any medium, provided the original work is properly cited. |
repository_type |
Open Access Journal |
institution_category |
Foreign Institution |
institution |
US National Center for Biotechnology Information |
building |
NCBI PubMed |
collection |
Online Access |
language |
English |
format |
Online |
author |
Bureau, Christophe Hanoun, Naima Torrisani, Jérôme Vinel, Jean-Pierre Buscail, Louis Cordelier, Pierre |
spellingShingle |
Bureau, Christophe Hanoun, Naima Torrisani, Jérôme Vinel, Jean-Pierre Buscail, Louis Cordelier, Pierre Expression and Function of Kruppel Like-Factors (KLF) in Carcinogenesis |
author_facet |
Bureau, Christophe Hanoun, Naima Torrisani, Jérôme Vinel, Jean-Pierre Buscail, Louis Cordelier, Pierre |
author_sort |
Bureau, Christophe |
title |
Expression and Function of Kruppel Like-Factors (KLF) in Carcinogenesis |
title_short |
Expression and Function of Kruppel Like-Factors (KLF) in Carcinogenesis |
title_full |
Expression and Function of Kruppel Like-Factors (KLF) in Carcinogenesis |
title_fullStr |
Expression and Function of Kruppel Like-Factors (KLF) in Carcinogenesis |
title_full_unstemmed |
Expression and Function of Kruppel Like-Factors (KLF) in Carcinogenesis |
title_sort |
expression and function of kruppel like-factors (klf) in carcinogenesis |
description |
Krüppel-like factor (KLF) family members share a three C2H2 zinc finger DNA binding domain, and are involved in cell proliferation and differentiation control in normal as in pathological situations. Studies over the past several years support a significant role for this family of transcription factors in carcinogenesis. KLFs can both activate and repress genes that participate in cell-cycle regulation. Among them, many up-regulated genes are inhibitors of proliferation, whereas genes that promote cell proliferation are repressed. However, several studies do present KLFs as positive regulator of cell proliferation. KLFs can be deregulated in multiple cancers either by loss of heterozygosity (LOH), somatic mutation or transcriptional silencing by promoter hypermethylation. Accordingly, KLF expression was shown to mediate growth inhibition when ectopically expressed in multiple cancer-derived cell lines through the inhibition of a number of key oncogenic signaling pathways, and to revert the tumorogenic phenotype in vivo. Taken together, these observations suggest that KLFs act as tumor suppressor. However, in some occasion, KLFs could act as tumor promoters, depending on “cellular context”. Thus, this review will discuss the roles and the functions of KLF family members in carcinogenesis, with a special focus on cancers from epithelial origin. |
publisher |
Bentham Science Publishers Ltd. |
publishDate |
2009 |
url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2729999/ |
_version_ |
1611442430073110528 |