Krüppel-like factor 4 (KLF4) regulates the miR-183~96~182 cluster under physiologic and pathologic conditions

Segura, Miguel F.; Jubierre, Luz; Li, SiDe; Soriano, Aroa; Koetz, Lisa; Gaziel-Sovran, Avital; Masanas, Marc; Kleffman, Kevin; Dankert, John F.; Walsh, Martin J.; Hernando, Eva

doi:10.18632/oncotarget.15459

Cited by 14 publications

(10 citation statements)

References 52 publications

(60 reference statements)

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“…however, studies with greater samples and in different stages to know the role in CRC progression were necessary. In a recent study, miR-10b was found to target Kruppel Like Factor 4 (KLF4), resulting in a classically metastatic and aggressive phenotype (36), but the molecular mechanism in CRC is not known. The zinc finger E-box binding homeobox 1 (ZEB1) protein is the main element in EMT (37).…”

Section: Epithelial-mesenchymal Transitionmentioning

confidence: 99%

“…The transcription factor TWIST-1 has also been reported to induce miR-10b, which promotes metastasis by targeting Homeobox D10 (HOXD10), which is associated with the inhibition of cell migration and may reduce E-cadherin expression, resulting in EMT ( 35 ); this mechanism is associated with hypermethylation of the miR-10 promoter in CRC tissues; however, studies with greater samples and in different stages to know the role in CRC progression were necessary. In a recent study, miR-10b was found to target Kruppel Like Factor 4 (KLF4), resulting in a classically metastatic and aggressive phenotype ( 36 ), but the molecular mechanism in CRC is not known.…”

Section: Epithelial–mesenchymal Transitionmentioning

confidence: 99%

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Colorectal Cancer Stem Cells in the Progression to Liver Metastasis

et al. 2020

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Colorectal carcinoma (CRC) is a leading cause of cancer mortality. Tumorigenesis is a dynamic process wherein cancer stem cells (CSCs) and their microenvironment promote initiation, progression, and metastasis. Metastatic colonization is an inefficient process that is very complex and is poorly understood; however, in most cases, metastatic disease is not curable, and resistance mechanisms tend to develop against conventional treatments. An understanding of the underlying mechanisms and factors that contribute to the development of metastasis in CRC can aid in the search for specific therapeutic targets for improving standard treatments. In this review, we summarize current knowledge regarding tumor biology and the use of stroma cells as prognostic factors and inflammatory inducers associated with the use of tumor microenvironments as a promoter of cancer metastasis. Moreover, we look into the importance of CSC, pericytes, and circulating tumor cells as mechanisms that lead to liver metastasis, and we also focus on the cellular and molecular pathways that modulate and regulate epithelial-mesenchymal transition. Finally, we discuss a novel therapeutic target that can potentially eliminate CSCs as a CRC treatment.

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Section: Epithelial-mesenchymal Transitionmentioning

confidence: 99%

Section: Epithelial–mesenchymal Transitionmentioning

confidence: 99%

Colorectal Cancer Stem Cells in the Progression to Liver Metastasis

et al. 2020

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“…Patients with depression and animal models of depression show changes in miRNA expression (Dwivedi, 2011 , 2016 ; Chan and Kocerha, 2012 ; Ma et al, 2016 ) as well as the levels of transcription factors, such as KLF11 and R1 (Johnson et al, 2011 ; Harris et al, 2015 ). It has been reported that KLF3 and KLF4 regulate the expression levels of miR-182 (Sachdeva et al, 2015 ; Segura et al, 2017 ), indicating that KLF family of proteins may regulate the expression levels of miRNAs and further modulate the downstream signaling of the pathway. Therefore, it is plausible to hypothesize that KLF11 could regulate the expression of miRNAs in the brain and influence the regulation of MAO-A.…”

Section: Possible Mechanism Of Mao-a Regulation By Mirnasmentioning

confidence: 99%

Potential Roles of microRNAs in the Regulation of Monoamine Oxidase A in the Brain

Higuchi

Soga

Parhar

2018

Front. Mol. Neurosci.

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Monoamine oxidase A (MAO-A) is an enzyme that regulates the levels of monoamine neurotransmitters, such as serotonin, noradrenaline and dopamine and it has been used as a therapeutic target for depression. However, MAO-A inhibitors, which directly acts on MAO-A protein, have limited use due to their adverse effects. microRNAs (miRNAs) are 18–22 nucleotide long, small non-coding RNAs, which have recently emerged as regulators of protein levels that could potentially be new therapeutic targets for psychiatric disorders. This review article aims to discuss the current status of the treatment for depression with MAO-A inhibitors and the regulatory factors of MAO-A. Further, the review also proposes possible regulatory mechanisms of MAO-A by miRNAs, which leads to better understanding of the pathology of depressive disorders and their potential use as therapeutic agents.

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“…Numerous studies have demonstrated that dysregulation of miRs contributes to the tumorigenesis and progression in many cancer types including NPC and can be associated with prognosis [6][7][8]. As a member of the highly conserved miR-183-96-182 cluster [9], miR-182 is located on human chromosome 7q32.2 [10]. And recent data show that miR-182 may play an oncogenic role in many human cancers, including the breast [11,12], colorectal [13], prostate [14] and bladder cancer [15].…”

Section: Introductionmentioning

confidence: 99%

M i R -182-5p I nduced by HIF-1α Promotes Tumorigenesis and Metastasis via Targeting ZFP36L1 in Nasopharyngeal Carcinoma

Wang¹,

Zhou²,

Ou³

et al. 2021

Preprint

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Accumulating evidence indicates that dysregulation of human microRNAs could serve as diagnostic and prognostic biomarkers in nasopharyngeal carcinoma (NPC). In the present study, we found that up-regulation of miR-182-5p was significantly associated with tumor development and poor prognosis in patients with NPC. Functional study demonstrated that miR-182-5p overexpression enhanced, whereas suppression of miR-182-5p impeded NPC cell proliferation, migration, tumorigenesis and metastasis. Mechanistically, miR-182-5p interacted with ZFP36 ring finger protein like 1 (ZFP36L1) at two sites in its 3’ un-translated region (UTR) and repressed ZFP36L1 expression in NPC. Consistently, an inverse correlation was observed between the expression levels of miR-182-5p and ZFP36L1 using clinical NPC primary tissues, and down-regulation of ZFP36L1 in NPC predicts poor survival. Furthermore, overexpression of miR-182-5p in NPC was attributable to the transcriptional activation effect induced by hypoxia-inducible factor 1α (HIF-1α). Taken together, our data suggest that miR-182-5p facilitates NPC development and progression through its ability to down-regulate ZFP36L1 expression, and that the HIF-1α/miR-182-5p/ZFP36L1 axis may serve as a novel therapeutic target in the management of NPC.

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Krüppel-like factor 4 (KLF4) regulates the miR-183~96~182 cluster under physiologic and pathologic conditions

Cited by 14 publications

References 52 publications

Colorectal Cancer Stem Cells in the Progression to Liver Metastasis

Colorectal Cancer Stem Cells in the Progression to Liver Metastasis

Potential Roles of microRNAs in the Regulation of Monoamine Oxidase A in the Brain

M i R -182-5p I nduced by HIF-1α Promotes Tumorigenesis and Metastasis via Targeting ZFP36L1 in Nasopharyngeal Carcinoma

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