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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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The Wilms' tumor blastema propagating cell is a self-renewing committed epithelial stem cell

ABSTRACT: Recently the cancer stem cell (CSC) model has been put forward to describe how a subset of cells within the tumor is responsible for tumor growth and heterogeneity. Wilms' tumor (WT), the most common pediatric renal malignancy, arises from developmentally arrested early renal progenitors. WT NCAM1+ALDH1+ CSCs have been recently isolated and shown to localize to tumor blastema. Herein by generating 'blastema'-only WT xenografts composed solely by cells expressing the SIX2 and NCAM1 embryonic renal stem cell markers, we surprisingly show that sorted ALDH1+ WT CSCs are phenotypically not the earliest renal stem cells. Rather, gene expression and proteomic comparative analysis disclose a more differentiated self-renewing epithelial cell type than bulk of the blastema. Thus, WT CSCs do not represent the transformed counterpart of the most primitive renal stem cell being more differentiated than the presumable WT cell of origin and are likely to de-differentiate to propagate the tumor blastema. We used Wilms tumor Xns, as well as, fetal renal tissue originally obtained from a patients or aborted fetus

ORGANISM(S): Homo sapiens

SUBMITTER: jasmine jacob

PROVIDER: E-GEOD-57269 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The Wilms' tumor blastema propagating cell is a self-renewing committed epithelial stem cell

Project description:Recently the cancer stem cell (CSC) model has been put forward to describe how a subset of cells within the tumor is responsible for tumor growth and heterogeneity. Wilms' tumor (WT), the most common pediatric renal malignancy, arises from developmentally arrested early renal progenitors. WT NCAM1+ALDH1+ CSCs have been recently isolated and shown to localize to tumor blastema. Herein by generating 'blastema'-only WT xenografts composed solely by cells expressing the SIX2 and NCAM1 embryonic renal stem cell markers, we surprisingly show that sorted ALDH1+ WT CSCs are phenotypically not the earliest renal stem cells. Rather, gene expression and proteomic comparative analysis disclose a more differentiated self-renewing epithelial cell type than bulk of the blastema. Thus, WT CSCs do not represent the transformed counterpart of the most primitive renal stem cell being more differentiated than the presumable WT cell of origin and are likely to de-differentiate to propagate the tumor blastema.

2015-12-31 | GSE57269 | GEO

Dissecting stages of human kidney development and Tumorigenesis with surface markers affords simple prospective Purification of nephron stem cells

Project description:When assembling a nephron during development a multipotent stem cell pool becomes restricted as differentiation ensues. A faulty differentiation arrest in this process leads to transformation and initiation of a Wilms' tumor. Mapping these transitions with respective surface markers affords accessibility to specific cell subpopulations. NCAM1 and CD133 have been previously suggested to mark human renal progenitor populations. Herein, using cell sorting, RNA sequencing, in vitro studies with serum-free media and in vivo xenotransplantation we demonstrate a sequential map that links human kidney development and tumorigenesis; In nephrogenesis, NCAM1+CD133- marks SIX2+ multipotent renal stem cells transiting to NCAM1+CD133+ differentiating segment-specific SIX2- epithelial progenitors and NCAM1-CD133+ differentiated nephron cells. In tumorigenesis, NCAM1+CD133- marks SIX2+ blastema that includes the ALDH1+ WT cancer stem/initiating cells, while NCAM1+CD133+ and NCAM1-CD133+ specifying early and late epithelial differentiation, are severely restricted in tumor initiation capacity and tumor self-renewal. Thus, negative selection for CD133 is required for defining NCAM1+ nephron stem cells in normal and malignant nephrogenesis. Human fetal kidney mRNA profiles of 3 cell populations (NCAM1+/CD133-, NCAM+/CD133+, NCAM-/CD133+) were generated by deep sequencing using Illumina HiSeq.

2016-04-01 | E-GEOD-78502 | biostudies-arrayexpress

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m1A marks translation initiation sites in human and mouse messenger RNA [microarray]

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Activation of a NCAM1 expressing progenitor cell population in adult human kidney epithelia

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SETD4 marks Quiescent Cancer Stem Cells with Chemoradiotherapy Resistance in Breast Cancer of MMTV-PyMT Mouse

Project description:We isolated quiescent CSCs using chemoradiotherapy resistance assays on tumors of MMTV-PyMT transgenic (specific breast cancer model) mice. We found that quiescent CSCs specifically expressed SETD4 without exception, and beyond activation exhibited high capacity of tumor-initiation in vivo and tumorsphere formation in vitro. Quiescent CSCs expressed high levels of ALDH1 and CD44 and low levels of CD24, that corresponds with their use as breast CSCs markers. Quiescent CSCs were showed to be resistant and able to survive under chemoradiotherapy treatment in either in vivo or in vitro models. Similarly, SETD4 overexpression caused cells extracted from tumors to exhibit clear chemoradiotherapy resistance. Transcriptomic analysis revealed that the molecular processes associated with cellular quiescence included those of DNA damage response and the Wnt/β-catenin signaling pathway. Together with our previous results, these findings showed that SETD4 marks quiescent CSCs and suggest that SETD4-marked quiescent CSCs could be used as key targets in clinical treatment for multiple cancers.

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