Kruppel-like factor 4 (KLF-4) inhibits the epithelial-to-mesenchymal transition and proliferation of human endometrial carcinoma cells

Wang, Xiaoli; Li, Xiaoyan; Huang, Cuiping; Li, Lei; Qu, Hongmei; Yu, Xiaoyan; Ni, Huijie; Cui, Qing

doi:10.3109/09513590.2016.1163673

Cited by 5 publications

(3 citation statements)

References 28 publications

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“…This phosphorylation induced nuclear entry was found to be critical for E47 to promote EMT and colon cancer metastasis (113). Krüppel-like factor family of Transcription Factors: Krüppel-like factor 4 (KLF4) has been shown to act as a negative regulator of EMT or even inducer of MET in a wide variety of cell/tissue types by different laboratories (114)(115)(116)(117)(118)(119)(120)(121)(122)(123). In fact, KLF4 expression was found to be downregulated in cells undergoing EMT in presence of TGFβ.…”

Section: Bhlh Family Transcription Factors: Twist Family Proteinsmentioning

confidence: 99%

Epithelial–mesenchymal transition and its transcription factors

et al. 2021

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Epithelial-mesenchymal transition or EMT is an extremely dynamic process involved in conversion of epithelial cells into mesenchymal cells, stimulated by an ensemble of signaling pathways, leading to change in cellular morphology, suppression of epithelial characters and acquisition of properties such as enhanced cell motility and invasiveness, reduced cell death by apoptosis, resistance to chemotherapeutic drugs etc. Significantly, EMT has been found to play a crucial role during embryonic development, tissue fibrosis and would healing, as well as during cancer metastasis. Over the years, work from various laboratories have identified a rather large number of transcription factors including the master regulators of EMT, with the ability to regulate the EMT process directly. In this review, we put together these EMT transcription factors and discussed their role in the process. We have also tried to focus on their mechanism of action, their inter-dependency, and the large regulatory network they form. Subsequently, it has become clear that the composition and structure of the transcriptional regulatory network behind EMT probably varies based upon various physiological and pathological contexts, or even in a cell/tissue type dependent manner.

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Section: Bhlh Family Transcription Factors: Twist Family Proteinsmentioning

confidence: 99%

Epithelial–mesenchymal transition and its transcription factors

et al. 2021

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“…EndoMT is required for ECC development, and KLF4 has been shown to inhibit or activate EndoMT 22,[40][41][42][43] . To decouple KLF4's role in EndoMT, we examined the expression patterns of Vimentin (Vim, mesenchymal marker) and Kinase Insert Domain Receptor (Kdr, endothelial marker) to test whether KLF4-low cells in the center of the AVC were more or less likely to undergo EndoMT.…”

Section: Klf4 Expression Negatively Correlates With Cushion Endomt Pr...mentioning

confidence: 99%

Endocardial primary cilia and blood flow are required for regulation of EndoMT during endocardial cushion development

Berg,

Gorham,

Lundt

et al. 2024

Preprint

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Blood flow is critical for heart valve formation, and cellular mechanosensors are essential to translate flow into transcriptional regulation of development. Here, we identify a role for primary cilia in vivo in the spatial regulation of cushion formation, the first stage of valve development, by regionally controlling endothelial to mesenchymal transition (EndoMT) via modulation of Kruppel-like Factor 4 (Klf4). We find that high shear stress intracardiac regions decrease endocardial ciliation over cushion development, correlating with KLF4 downregulation and EndoMT progression. Mouse embryos constitutively lacking cilia exhibit a blood-flow dependent accumulation of KLF4 in these regions, independent of upstream left right abnormalities, resulting in impaired cushion cellularization. snRNA-seq revealed that cilia KO endocardium fails to progress to late-EndoMT, retains endothelial markers and has reduced EndoMT/mesenchymal genes that KLF4 antagonizes. Together, these data identify a mechanosensory role for endocardial primary cilia in cushion development through regional regulation of KLF4.

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“…klf2 -/or klf5 -/mice die in utero during embryonic life (29,30). Previous studies have revealed that KLFs participate in proliferation, apoptosis, epithelial-mesenchymal transition (EMT), angiogenesis and other malignant biological behavior of cancer (14,(31)(32)(33). KLF4 inhibits EMT and proliferation of endometrial cancer cells, whilst KLF8 promotes EMT and proliferation of bladder cancer cells (34,35); these findings suggest that the KLF gene family may serve a critical role in cancer genesis and prognosis.…”

Section: Bioinformatics Analysis Of Klf2 As a Potential Prognostic Fa...mentioning

confidence: 99%

Bioinformatics analysis of KLF2 as a potential prognostic factor in ccRCC and association with epithelial‑mesenchymal transition

Ren

Wang

et al. 2022

Exp Ther Med

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Clear cell renal cell carcinoma (ccRCC) is a primary pathological subtype of RCC and has poor clinical outcome. Krüppel-like factors (KLFs), which are zinc-finger proteins, may be involved in ccRCC development and progression. KLFs belong to the zinc-finger family of DNA-binding transcription factors and regulate transcription of downstream target genes. KLFs are involved in cancer development. The present study aimed to investigate the role of KLFs in ccRCC prognosis. The Cancer Genome Atlas database and multifactorial analysis showed that KLFs were widely expressed in pan-cancers and KLF2 was an independent protective factor for ccRCC prognosis. Patients with low KLF2 expression had a low survival probability and expression of KLF2 was downregulated in patients with ccRCC with high pathological grade (II + III vs. I). In addition, western blot and reverse transcription-quantitative PCR revealed that KLF2 was expressed at low levels in ccRCC cell lines and overexpression of KLF2 inhibited cell migration. In addition, KLF2 expression was negatively correlated with methylation. KLF2 expression was elevated following treatment of ccRCC cells with DNA methyltransferase inhibitor. A prognostic risk index prediction model was constructed based on multiple Cox regression. The receiver operating characteristic curve was 0.780 (area under curve >0.5). Furthermore, Gene Ontology enrichment analysis showed that 'cell adhesion' and 'junction' were negatively correlated with KLF2 and that high-risk group exhibited significantly activated 'epithelial-mesenchymal transition'. Western blot analysis showed that overexpression of KLF2 increased expression of E-cadherin, while decreasing levels of N-cadherin and vimentin. The present study highlighted the role of KLFs in ccRCC prognosis prediction and provides a research base for the search of validated prognostic biological markers for ccRCC.

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Kruppel-like factor 4 (KLF-4) inhibits the epithelial-to-mesenchymal transition and proliferation of human endometrial carcinoma cells

Cited by 5 publications

References 28 publications

Epithelial–mesenchymal transition and its transcription factors

Epithelial–mesenchymal transition and its transcription factors

Endocardial primary cilia and blood flow are required for regulation of EndoMT during endocardial cushion development

Bioinformatics analysis of KLF2 as a potential prognostic factor in ccRCC and association with epithelial‑mesenchymal transition

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