Snail Family Members Unequally Trigger EMT and Thereby Differ in Their Ability to Promote the Neoplastic Transformation of Mammary Epithelial Cells

Gras, Baptiste; Jacqueroud, Laurent; Wierinckx, Anne; Lamblot, Christelle; Fauvet, Frédérique; Lachuer, Joël; Puisieux, Alain; Ansieau, Stéphane

doi:10.1371/journal.pone.0092254

Cited by 45 publications

(47 citation statements)

References 53 publications

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“…It was reported that SNAI1 could induce EndMT under certain conditions [14,15,17,[39][40][41][42]. Besides, SNAI1 also had a role in embryonic vessel formation and in vitro angiogenesis [19,20].…”

Section: Discussionmentioning

confidence: 97%

SNAI1, an endothelial–mesenchymal transition transcription factor, promotes the early phase of ocular neovascularization

Sun

Chang

et al. 2018

Angiogenesis

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Ocular neovascularization is a comprehensive process involved in retinal vascular development and several blinding diseases such as age-related macular degeneration and retinopathy of prematurity, with vascular endothelial growth factor (VEGF) regarded as the master regulator. However, the qualified effect of anti-VEGF therapy reveals that the underlying mechanisms are still not clearly identified. To initialize angiogenesis, endothelial cells undergo a phenotype switching to generate highly migratory and invasive cells. This process shares certain similar characters observed in endothelial-mesenchymal transition (EndMT). Here, we found that SNAI1, an EndMT transcription factor, was expressed by endothelial cells in both physiological and pathological ocular neovascularization. SNAI1 overexpression triggered cell morphological change and enhanced cell motility, while loss of SNAI1 attenuated migration, invasion and sprouting. RNA sequence analysis further revealed that SNAI1 knockdown decreased the expression of genes related to cytoskeleton rearrangement and ECM remodeling. Moreover, intravitreal injection of small interfering RNA of SNAI1 suppressed new vessel formation in developing retina as well as mice model of choroidal neovascularization and oxygen-induced retinopathy. Therefore, we propose that the EndMT transcription factor SNAI1 promotes the early phase of ocular neovascularization and may provide a potential therapeutic target.

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Section: Discussionmentioning

confidence: 97%

SNAI1, an endothelial–mesenchymal transition transcription factor, promotes the early phase of ocular neovascularization

Sun

Chang

et al. 2018

Angiogenesis

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“…Infections were performed as described in [64]. Infected cells were selected with puromycin (1 μg/ml) before being plated in ultra-low adherent conditions or plated on soft agar.…”

Section: Methodsmentioning

confidence: 99%

ABCG2, a novel antigen to sort luminal progenitors of BRCA1- breast cancer cells

et al. 2014

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IntroductionTumor-initiating cells (TICs), aka “cancer stem cells”, are believed to fuel tumors and to sustain therapy resistance and systemic metastasis. Breast cancer is the first human carcinoma in which a subpopulation of cells displaying a specific CD44+/CD24-/low/ESA+ antigenic phenotype was found to have TIC properties. However, CD44+/CD24-/low/ESA+ is not a universal marker phenotype of TICs in all breast cancer subtypes. The aim of this study was to identify novel antigens with which to isolate the TIC population of the basal-A/basal-like breast cancer cell lines.MethodsWe used polychromatic flow-cytometry to characterize the cell surface of several breast cancer cell lines that may represent different tumor molecular subtypes. We next used fluorescence-activated cell sorting to isolate the cell subpopulations of interest from the cell lines. Finally, we explored the stem-like and tumorigenic properties of the sorted cell subpopulations using complementary in vitro and in vivo approaches: mammosphere formation assays, soft-agar colony assays, and tumorigenic assays in NOD/SCID mice.ResultsThe CD44+/CD24+ subpopulation of the BRCA1-mutated basal-A/basal-like cell line HCC1937 is enriched in several stemness markers, including the ABCG2 transporter (i.e., the CD338 antigen). Consistently, CD338-expressing cells were also enriched in CD24 expression, suggesting that coexpression of these two antigenic markers may segregate TICs in this cell line. In support of ABCG2 expression in TICs, culturing of HCC1937 cells in ultra-low adherent conditions to enrich them in precursor/stem-cells resulted in an increase in CD338-expressing cells. Furthermore, CD338-expressing cells, unlike their CD338-negative counterparts, displayed stemness and transformation potential, as assessed in mammosphere and colony formation assays. Lastly, CD338-expressing cells cultured in ultra-low adherent conditions maintained the expression of CD326/EpCAM and CD49f/α6-integrin, which is a combination of antigens previously assigned to luminal progenitors.ConclusionCollectively, our data suggest that CD338 expression is specific to the tumor-initiating luminal progenitor subpopulation of BRCA1-mutated cells and is a novel antigen with which to sort this subpopulation.Electronic supplementary materialThe online version of this article (doi:10.1186/1476-4598-13-213) contains supplementary material, which is available to authorized users.

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“…Out of these five genes, ROR1, SNAI3, TET1, TSPAN13 were significantly upregulated in metastatic compared with primary ( Figure 5). Upregulation of ROR1 in melanoma was reported recently [34], while overexpression of TSPAN13 was reported in other cancers [35] and SNAI3 involved in the EMT process, however, its role in melanoma is not well documented yet [36]. Intriguingly, loss of 5-hydroxymethylcytosine and downregulation of TET1 in melanoma compared with nevi was reported as a key feature of melanoma [37].…”

Section: Mir-193bmentioning

confidence: 95%

Scan_Tcga Tools for Integrated Epigenomic and Transcriptomic Analysis of Tumor Subgroups

et al. 2016

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Aim:The Cancer Genome Atlas contains multiple levels of genomic data (mutation, gene expression, DNA methylation, copy number variation) for 33 cancer types for almost 11,000 patients. However, a dearth of appropriate software tools makes it difficult for bench scientists to use these data effectively. Materials & methods: Here, we present a suite of flexible, fast and command line-based scripts that will allow retrieval and analysis of DNA methylation (tool: scan_tcga_methylation.awk), mRNA (tool: scan_tcga_mRNA.awk) and miRNA expression (tool: scan_tcga_miRNAs.awk) from cancer genome atlas network level 3 data. Results: We demonstrate the utility of these tools by analyzing DNA methylation and mRNA expression signatures of 60 frequently deregulated cancer genes and also of 30 miRNAs in primary (n = 102) and metastatic melanoma patients (n = 367). Conclusion: Our analysis illustrates the validity of the scan_tcga tools and reveals the epigenomic signatures and importance of identifying smaller patient subgroups with distinct molecular profiles.

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Snail Family Members Unequally Trigger EMT and Thereby Differ in Their Ability to Promote the Neoplastic Transformation of Mammary Epithelial Cells

Cited by 45 publications

References 53 publications

SNAI1, an endothelial–mesenchymal transition transcription factor, promotes the early phase of ocular neovascularization

SNAI1, an endothelial–mesenchymal transition transcription factor, promotes the early phase of ocular neovascularization

ABCG2, a novel antigen to sort luminal progenitors of BRCA1- breast cancer cells

Scan_Tcga Tools for Integrated Epigenomic and Transcriptomic Analysis of Tumor Subgroups

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