Krüppel‐like factor 5 activates MEK/ERK signaling via EGFR in primary squamous epithelial cells

@article{Yang2007KrppellikeF5,
  title={Kr{\"u}ppel‐like factor 5 activates MEK/ERK signaling via EGFR in primary squamous epithelial cells},
  author={Yizeng Yang and Bree G. Goldstein and Hiroshi Nakagawa and Jonathan P Katz},
  journal={The FASEB Journal},
  year={2007},
  volume={21},
  pages={543 - 550}
}
Rapid cell proliferation is a hallmark of transit amplifying cells, but the mechanisms of this localized proliferation are not well understood. The Krüppel‐like factor family member Klf5 (IKLF; BTEB2) promotes cell proliferation and is highly expressed in squamous epithelia, in regions of active proliferation. Here, using mouse primary esophageal keratinocytes as a model, we identify a critical role for Klf5 in regulating squamous epithelial proliferation via the epidermal growth factor… 
View on Wiley
med.upenn.edu
82 Citations
Highly Influential Citations
4
Background Citations
31
Methods Citations
4
Results Citations
2

82 Citations

Citation Type

Citation Type

Krüppel-like Factor 5 Controls Keratinocyte Migration via the Integrin-linked Kinase*
TLDR
It is demonstrated that Klf5 is a key regulator of cell migration via ILK and provide new insight into the regulation of epithelial cell migration.
Up-Regulation of Krüppel-Like Factor 5 in Pancreatic Cancer Is Promoted by Interleukin-1β Signaling and Hypoxia-Inducible Factor-1α
TLDR
In conclusion, overexpression of KLF5 in human pancreatic cancer cells is not mediated by KRAS/Raf/MAPK/Erk signaling, but involves the IL-1β/IL-1R system, p38, and the transcription factor HIF-1α.
Essential role of KLF5 transcription factor in cell proliferation and differentiation and its implications for human diseases
TLDR
The expression of KLF5 is frequently abnormal in human cancers and in cardiovascular disease-associated vascular smooth muscle cells (VSMCs) and could be a potential diagnostic biomarker and therapeutic target for cancer and cardiovascular diseases.
KLF4 transcriptionally activates non-canonical WNT5A to control epithelial stratification
TLDR
WNT5A, a non-canonical Wnt ligand implicated in epithelial differentiation, repair, and cancer, is defined as a direct transcriptional target that is activated by KLF4 in squamous epithelial cells and delineated a novel pathway for epithelial differentiated and stratification.
Investigation of KLF5 Function in Normal Hematopoiesis.
TLDR
The data in the Klf 5 conditional KO model are consistent with Klf5 playing a role in growth and differentiation in the myeloid lineage, as suggested by in vitro data, and further suggests that Klf4 may have roles in multiple haematopoietic lineages.
Krüppel-like factor 5 promotes breast cell proliferation partially through upregulating the transcription of fibroblast growth factor binding protein 1
TLDR
It is demonstrated that KLF5 binds and activates the FGF-BP promoter through a GC box by luciferase reporter, oligo pull down and chromatin immunoprecipitation (ChIP) assays, suggesting that KLf5 may promote breast cancer cell proliferation at least partially through directly activating the F GF-BP mRNA transcription.
Overexpression of Kruppel-like factor 5 in esophageal epithelia in vivo leads to increased proliferation in basal but not suprabasal cells.
TLDR
While Klf5 positively regulates proliferation in basal cells, it is not sufficient to maintain proliferation in the esophageal epithelium.
Restoring KLF5 in esophageal squamous cell cancer cells activates the JNK pathway leading to apoptosis and reduced cell survival.
TLDR
Restoration of Krüppel-like factor 5 in ESCC cells promotes apoptosis and decreases cell survival in a JNK-dependent manner, providing a potential therapeutic target for human ESCC.
KLF4 activates NFκB signaling and esophageal epithelial inflammation via the Rho-related GTP-binding protein RHOF
TLDR
It is demonstrated that the Rho-related GTP-binding protein RHOF is activated by KLF4 in esophageal keratinocytes, leading to the induction of NFκB signaling, which provides a potentially important and clinically-relevant mechanism for esphageal inflammation and inflammation-mediated esophagal squamous cell cancer.
Krüpple-Like Factor 5 Is Required for Proper Maintenance of Adult Intestinal Crypt Cellular Proliferation
TLDR
Tamoxifen-induced recombination directed by the epithelial-specific Villin promoter was used to delete Klf5 from the adult mouse intestine and results indicate that Klf 5 is necessary to maintain adult intestinal crypt proliferation and proper cellular differentiation.
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 48 REFERENCES
Krüppel-like factor 5 mediates the transforming activity of oncogenic H-Ras
TLDR
It is demonstrated that levels of KLF5 transcript and protein are significantly elevated in oncogenic H-Ras-transformed NIH3T3 cells and that the elevated level of KLf5 is in part responsible for the proproliferative and transforming activities of oncogens H- Ras.
Intestinal Tumor Progression Is Associated with Altered Function of KLF5*
TLDR
Data indicate that intestinal tumor progression is associated with a change in the growth-related functions of KLf5 and that intestinal tumors down-regulate KLF5 expression by multiple mechanisms.
Krüppel-like transcription factor KLF5 is a key regulator of adipocyte differentiation.
Krüppel‐like factor 5 promotes mitosis by activating the cyclin B1/Cdc2 complex during oncogenic Ras‐mediated transformation
KLF4 and KLF5 regulate proliferation, Apoptosis and invasion in esophageal cancer cells
TLDR
It is demonstrated that KLF4 and KLF5 are key players in a number of cellular processes critical for esophageal carcinogenesis by affecting proliferation, apoptosis, and invasion.
KLF5 promotes cell proliferation and tumorigenesis through gene regulationin the TSU‐Pr1 human bladder cancer cell line
TLDR
It is suggested that the KLF5 transcription factor plays an oncogenic role in the TSU‐Pr1 bladder cancer cell line through the regulation of a subset of genes.
Ubiquitin–proteasome degradation of KLF5 transcription factor in cancer and untransformed epithelial cells
TLDR
It is shown that KLF5 is an unstable protein with a short half-life and ubiquitin-mediated proteolysis, and deletion of a 56-amino-acid sequence adjacent to a known transactivation domain of KLf5 significantly reduced its ubiquitination and degradation.
Epidermal Growth Factor Receptor Mediates Increased Cell Proliferation, Migration, and Aggregation in Esophageal Keratinocytes in Vitro and in Vivo *
TLDR
The functional effects of EGFR overexpression help to explain its role in the initiating steps of esophageal squamous carcinogenesis.
Intestinal-enriched Krüppel-like Factor (Krüppel-like Factor 5) Is a Positive Regulator of Cellular Proliferation*
TLDR
It is shown that IKLF encodes a delayed early response gene product that positively regulates cellular proliferation and may give rise to a transformed phenotype when overexpressed.
Krüppel-like zinc-finger transcription factor KLF5/BTEB2 is a target for angiotensin II signaling and an essential regulator of cardiovascular remodeling
TLDR
KLF5 seems to be a key element linking external stress and cardiovascular remodeling, and that in vivo administration of RAR ligands affected stress responses in the cardiovascular system in a KLF5-dependent manner.
...
1
2
3
4
5
...