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Journal ArticleDOI

Krüppel-like factors in cancer

TLDR
The roles and regulation of the 17 known KLFs in various cancer-relevant processes are discussed, with some KLFs having different roles in normal cells and cancer, during cancer development and progression and in different cancer types.
Abstract
Kruppel-like factors (KLFs) are a family of DNA-binding transcriptional regulators with diverse and essential functions in a multitude of cellular processes, including proliferation, differentiation, migration, inflammation and pluripotency. In this Review, we discuss the roles and regulation of the 17 known KLFs in various cancer-relevant processes. Importantly, the functions of KLFs are context dependent, with some KLFs having different roles in normal cells and cancer, during cancer development and progression and in different cancer types. We also identify key questions for the field that are likely to lead to important new translational research and discoveries in cancer biology.

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Journal ArticleDOI

Cancer-derived exosomal miR-25-3p promotes pre-metastatic niche formation by inducing vascular permeability and angiogenesis.

TL;DR: It is shown that colorectal cancer (CRC) derived exosomal miR-25-3p promotes vascular leakiness and angiogenesis, CRC metastasis, and is upregulated in CRC pateints with metastasis.
Journal ArticleDOI

Nrf2 Amplifies Oxidative Stress via Induction of Klf9

TL;DR: It is demonstrated that Klf9 independently causes increased ROS levels in various types of cultured cells and in mouse tissues and is required for pathogenesis of bleomycin-induced pulmonary fibrosis in mice and identified as a ubiquitous regulator of oxidative stress and lung injury.
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Interplay between arginine methylation and ubiquitylation regulates KLF4-mediated genome stability and carcinogenesis.

TL;DR: A critical role is pointed to for aberrant KLF4 regulation by PRMT5 in genome stability and breast carcinogenesis through structure-based modelling and simulations.
Journal ArticleDOI

Krüppel-like factors in mammalian stem cells and development

TL;DR: An overview of Krüppel-like factors, a family of zinc-finger transcription factors that play fundamental roles in development and stem cell biology, as revealed by studies of animal models is provided.
References
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Journal ArticleDOI

The Krüppel-like factor 9 (KLF9) network in HEC-1-A endometrial carcinoma cells suggests the carcinogenic potential of dys-regulated KLF9 expression

TL;DR: Over-expression of KLF9 in the human endometrial cancer cell line HEC-1-A alters cell morphology, proliferative indices, and differentiation, when compared to KLF 9 under-expressing HECs, and the abundance of mRNAs that encode hypothetical proteins (KLF9-induced: C10orf38 and C9orf167) were altered by KLf9 expression.
Journal ArticleDOI

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

TL;DR: 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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Hepatocyte Growth Factor Enhances Alternative Splicing of the Krüppel-like Factor 6 (KLF6) Tumor Suppressor to Promote Growth through SRSF1

TL;DR: Enhanced cell replication through increased KLF6 alternative splicing is a novel growth-promoting pathway of HGF that could contribute to the molecule's mitogenic activity in physiologic liver growth and hepatocellular carcinoma.
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TIEG1 inhibits breast cancer invasion and metastasis by inhibition of epidermal growth factor receptor (EGFR) transcription and the EGFR signaling pathway.

TL;DR: In this paper, the authors found that decreased TIEG1 expression is associated with increased human epidermal growth factor receptor (EGFR) expression in breast cancer tissues and cell lines.
Journal ArticleDOI

Klf4 Overexpression Activates Epithelial Cytokines and Inflammation-Mediated Esophageal Squamous Cell Cancer in Mice

TL;DR: KLF4 has distinct functions in carcinogenesis; upregulation of Klf4 specifically in esophageal epithelial cells induces inflammation, and this mouse model might be used to determine the molecular mechanisms of esphageal squamous cell cancer and inflammation-mediated carcinogenesis.
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