SPROUTY-2 represses the epithelial phenotype of colon carcinoma cells via upregulation of ZEB1 mediated by ETS1 and miR-200/miR-150

Barbáchano, Antonio; Fernández‐Barral, Asunción; Перейра, Фернандо Лобо; Segura, Miguel F.; Ordóñez‐Morán, Paloma; Pau, Enrique Carrillo de Santa; González‐Sancho, José Manuel; Hanniford, Douglas; Martínez, Natàlia; Costales-Carrera, Alba; Real, Francisco X.; Pálmer, Héctor G.; Rojas, José M.; Hernando, Eva; Múñoz, Alberto

doi:10.1038/onc.2015.366

Cited by 43 publications

(44 citation statements)

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“…MiR-150-5p was revealed to target ZEB1 in various cancers such colon cancer [38], esophageal squamous cancer [37] and ovarian cancer [35], and ZFAS1 was demonstrated to sequestrate miR-150-5p and exerted its pro-metastatic activity in hepatocellular cancer [39]. First, we constructed ZEB1 3’UTR wild type or mutated (predicted miR-150 binding sites) luciferase plasmids in the pmirGLO dual luciferase reporter vector, and luciferase activity was evaluated after co-transfection of miRNA and luciferase plasmids.…”

Section: Resultsmentioning

confidence: 99%

“…Repression of E-cadherin expression is an important phenotype in EMT, while ZEB1 is a major transcriptional suppressor for E-cadherin via binding to the E-box in the promoter of CDH1 gene directly [54]. Recently, several miRNAs such as miR-200 family and miR-150-5p were confirmed to target ZEB1 and caused mRNA degradation, thus blocking EMT [35–38]. As another type of ncRNA, lncRNAs are emerging as important regulators in various biological and disease development processes [2].…”

Section: Discussionmentioning

confidence: 99%

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Long non-coding RNA linc00673 regulated non-small cell lung cancer proliferation, migration, invasion and epithelial mesenchymal transition by sponging miR-150-5p

et al. 2017

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BackgroundThe function of a new long non-coding RNA linc00673 remains unclear. While identified as an oncogenic player in non-small cell lung cancer (NSCLC), linc00673 was found to be anti-oncogenic in pancreatic ductal adenocarcinoma (PDAC). However whether linc00673 regulated malignancy and epithelial mesenchymal transition (EMT) has not been characterized.MethodsCell proliferation was assessed using CCK-8 and EdU assays, and cell migration and invasion were assessed using scratch assays and transwell invasion assays. Epithelial mesenchymal transition was examined using western blot, qRT-PCR and immunofluorescence staining. Interaction between miRNA and linc00673 was determined using luciferase reporter assays. In vivo experiments were performed to assess tumor formation. In addition, the expression data of NSCLC specimens of TCGA and patient survival data were utilized to explore the prognostic significance of linc00673.ResultsIn the present study, we found high linc00673 expression was associated with poor prognosis of NSCLC patients. In vitro experiments showed linc00673 knockdown reversed TGF-β induced EMT, and miR-150-5p was predicted to target linc00673 through bioinformatics tools. Overexpression of miR-150-5p suppressed lin00673’s expression while inhibition of miR-150-5p led to significant upregulation of lin00673, suggesting that linc00673 could be negatively regulated by miR-150-5p, which was further confirmed by the inverse correlation between linc00673 and miR-150-5p in NSCLC patients’ specimen. Furthermore, we proved that miR-150-5p could directly target linc00673 through luciferase assay, so linc00673 could sponge miR-150-5p and modulate the expression of a key EMT regulator ZEB1 indirectly. In addition, miR-150-5p inhibition abrogated linc00673 silence mediated proliferation, migration, invasion and EMT suppressing effect. Moreover, the inhibition of linc00673 significantly attenuated the tumorigenesis ability of A549 cells in vivo.ConclusionsWe validated linc00673 as a novel oncogenic lncRNA and demonstrated the molecular mechanism by which it promotes NSCLC, which will advance our understanding of its clinical significance.Electronic supplementary materialThe online version of this article (doi:10.1186/s12943-017-0685-9) contains supplementary material, which is available to authorized users.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA linc00673 regulated non-small cell lung cancer proliferation, migration, invasion and epithelial mesenchymal transition by sponging miR-150-5p

et al. 2017

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“…25 As mentioned previously, DICER is an enzyme involved in the cytoplasmic processing and maturation of microRNAs. The use of microRNA target prediction programs (e.g., TargetScan v7.1: www.targetscan.org, mirdb: www.mirdb.org, TarBase v8.0: http://carolina.…”

Section: Resultsmentioning

confidence: 94%

The role of the miR‐200 family in epithelial–mesenchymal transition in colorectal cancer: a systematic review

O’Brien

Carter

Burton

et al. 2018

Intl Journal of Cancer

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Colorectal cancer (CRC) is associated with significant morbidity and mortality as many patients are diagnosed with advanced stage disease. MicroRNAs are small, noncoding RNA molecules that have a major role in gene expression regulation and are dysregulated in CRC. The miR-200 family is involved in epithelial-mesenchymal transition (EMT). This systematic review describes the roles of the miR-200 family in EMT in CRC. A search of electronic databases (PubMed and Embase) was conducted between January 2000 and July 2017. Both in vitro and human studies reporting on the miR-200 family and CRC were included. Studies describing molecular pathways and the role of the miR-200 family in the diagnostic and therapeutic management of CRC were analyzed. Thirty-four studies (22 in vitro and 18 human studies) were included. miR-200 family expression is regulated epigenetically and via transcriptional factor regulation. In vitro studies show that transfection of miR-200 family members into chemo-resistant colon cancer cell lines results in improved chemo-sensitivity and epithelial phenotype restoration. There is intra-tumoral variability in the tissue expression of miR-200 family members with decreased expression at the invasive front. Clinical studies in CRC patients have shown decreased primary tumor tissue expression of miR-429, miR-200a and miR-200c may be associated with worse survival. Conversely, increased blood levels of miR-141, miR-200a and miR-200c may be associated with worse outcomes. The miR-200 family has a central role in EMT. The miR200 family has potential for both prognostic and therapeutic management of CRC.

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“…Of note, Epithelial-to mesenchymal transition (EMT) is a process in which epithelial cells acquire mesenchymal properties, and increased ability to invade and metastasize [33, 70]. Moreover, studies have now linked EMT with the acquisition of stem-cell characteristics and demonstrated important role of specific claudin proteins in regulating the EMT process, and cancer progression [3, 52]. In this regard, the key role of claudin-1 in regulating the EMT process is well documented.…”

Section: Introductionmentioning

confidence: 99%

Claudin proteins, outside-in signaling, and carcinogenesis

Singh¹,

Uppada

Dhawan³

2016

Pflugers Arch - Eur J Physiol

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Environment affects an individual’s development and disease risk which then suggest that the environmental cues must have ways of reaching to the cellular nuclei to orchestrate desired genetic changes. Polarized and differentiated epithelial cells join together by cell-cell adhesions to create a protective sheet which separates body’s internal milieu from its environment, albeit in highly regulated manner. Among these cell-cell adhesions, a key role of tight junction, the apical cell-cell adhesion, in maintaining epithelial cell polarity and differentiation is well recognized. Moreover, significant changes in expression and cellular distribution of claudin proteins, integral component of the tight junction, characterize pathophysiological changes including neoplastic growth and progression. Studies have further confirmed existence of complex claudin-based interactomes and demonstrated that changes in such protein partnering can influence barrier integrity and communication between a cell and its environment to produce undesired outcome. Cell signaling is the process by which cells respond to their environment to make dynamic decisions to live, grow and proliferate, or die. Thus, pivotal role of the deregulated tight junction structure/function in influencing cellular signaling cascades to alter cellular pheno-type can be envisaged, however, is not well understood. Needless to mention that advanced knowledge in this area can help improve therapeutic considerations and preventive measures. Here, we discuss potential role of the tight junction in the regulation of Boutside-in^ signaling to regulate cancer growth, with specific focus upon the claudin family of proteins.

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SPROUTY-2 represses the epithelial phenotype of colon carcinoma cells via upregulation of ZEB1 mediated by ETS1 and miR-200/miR-150

Abstract: Esta es la versión de autor del artículo publicado en: This is an author produced version of a paper published in:Oncogene 35.23 (2016)

Cited by 43 publications

References 60 publications

Long non-coding RNA linc00673 regulated non-small cell lung cancer proliferation, migration, invasion and epithelial mesenchymal transition by sponging miR-150-5p

Long non-coding RNA linc00673 regulated non-small cell lung cancer proliferation, migration, invasion and epithelial mesenchymal transition by sponging miR-150-5p

The role of the miR‐200 family in epithelial–mesenchymal transition in colorectal cancer: a systematic review

Claudin proteins, outside-in signaling, and carcinogenesis

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