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Gene expression changes with LGR5 knockdown in LoVo colon cancer cells

ABSTRACT: Gene expression changes with LGR5 knockdown in LoVo colon cancer cells

PROVIDER: PRJNA559893 | ENA |

REPOSITORIES: ENA

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Gene expression changes with LGR5 knockdown in LoVo colon cancer cells

Project description:The goal of this study was to identify gene expression changes in response to loss of LGR5 in the LoVo colon cancer cell line.

2019-08-13 | GSE135749 | GEO

Expression data from LoVo colon cancer lines +/- constitutive LIN28B expression

Project description:We sought to elucidate the molecular mechanisms whereby LIN28B functions by comparing the gene expression profile of cells constitutively expressing LIN28B to empty vector controls. Accordingly, we performed microarray analysis on total RNA isolated from empty vector LoVo and LIN28B-expressing LoVo colon cancer cell lines. Constitutive LIN28B expression was achieved in the LoVo (ATCC #CCL-229) colon cancer cell line via retroviral transduction of MSCV-PIG-LIN28B. Contol = empty vector MSCV-PIG.

2010-12-29 | E-GEOD-26334 | biostudies-arrayexpress

Expression data from LoVo colon cancer lines +/- constitutive LIN28B expression

2010-12-29 | GSE26334 | GEO

Expression data from xenograft tumors derived from LoVo colon cancer lines +/- constitutive LIN28B expression

Project description:We sought to elucidate functions of LIN28B and potential mechanisms whereby it may promote metastasis by comparing the gene expression profile of LIN28B metastases to primary tumors. Accordingly, we performed microarray analysis on total RNA isolated from empty vector tumors, LIN28B-LoVo tumors, and LIN28B-LoVo metastases Constitutive LIN28B expression was achieved in the LoVo (ATCC #CCL-229) colon cancer cell line via retroviral transduction of MSCV-PIG-LIN28B. xenografts were produced via injection of 1x106 cells subcutaneously into the rear flanks of nude mice. Microarrays were conducted on primary tumors from empty vector and LIN28B-expressing cells, as well as metastases derived from primary tumors constitutively expressing LIN28B. (Note: metastases did not occur with empty vector tumors)

2010-12-29 | E-GEOD-26335 | biostudies-arrayexpress

RNA-seq of LGR5(+) and LGR5(-) cells isolated from human colon adenoma organoids and targeted DNA-seq of a colorectal biobank

Project description:This study has two components: (1) Human colon adenoma organoids (n=4 patients) were dissociated into single cells. Cells were incubated with a magnetic bead bound to an LGR5 antibody and run through a magnetic column. Magnet bound cells and flow through negative (FTN) cells were obtained. Magnet bound and FTN cells were incubated with an APC-check reagent (which binds to the magnetic bead on the LGR5 antibody) and DAPI, before being sorted by flow cytometry. 3 populations of live (DAPI-) cells were collected: FTN: Flow through negative. LGR5 negative by magnet and by flow cytometry SortedNeg: Magnet bound cells that were negative for LGR5 by flow cytometry SortedPos: Magnet bound cells that were positive for LGR5 by flow cytometry (2) Human colon organoids, as well as the tissue the organoid was derived from and adjcacent normal tissue (from n=19) were also profiled for known colorectal cancer associated mutations using the Qiagen Qiaseq Colorectal Cancer Panel, which provides targeted sequencing information for 71 genes.

2020-04-30 | E-MTAB-4698 | biostudies-arrayexpress

Reg4+ Deep Crypt Secretory cells function as epithelial niche for Lgr5+ stem cells in colon

Project description:Lgr5+ stem cells reside at crypt bottoms of the small and large intestine. Small intestinal Paneth cells supply Wnt3, EGF and Notch signals to neighboring Lgr5+ stem cells. While the colon lacks Paneth cells, Deep Crypt Secretory (DCS) cells are intermingled with Lgr5+ stem cells at crypt bottoms. Here, we report Reg4 as a marker of DCS cells. To investigate a niche function, we eliminated DCS cells using the diphtheria-toxin receptor gene knocked into the murine Reg4 locus. Ablation of DCS cells results in loss of stem cells from colonic crypts and disrupts gut homeostasis and colon mini-gut formation. In agreement, sorted Reg4+ DCS cells promote organoid formation of single Lgr5+ colon stem cells. Stem cells are forced to generate DCS cells in vitro by combined Notch inhibition and Wnt activation. We conclude that Reg4+ DCS cells serve as Paneth cell equivalents in the colon crypt niche.

2016-10-05 | GSE63256 | GEO

microRNA array of LoVo cells and LoVo-Small Extracellular Vesicles

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2019-07-01 | GSE117866 | GEO

Gene expression profiles of HT29 cells in which LGR5 expression was suppressed.

Project description:GATA6 is a zinc finger transcription factor that is required for the proliferation, development and specific gene regulation in the gastrointestinal tract. We have recently reported that GATA6-mediated induction of the intestinal stem cell marker LGR5 is required for the tumorigenicity of colon cancer cells. However, knockdown of LGR5, unlike GATA6, does not affect the proliferation of these cells under adherent conditions. Here we show that REG4, a member of the regenerating islet-derived (REG) family, is a target of GATA6. We further demonstrate that REG4 is downregulated by overexpression of miR-363, which suppresses GATA6 expression. Moreover, we show that GATA6-mediated activation of REG4 causes an acceleration of the growth of colon cancer cells under adherent conditions. These results suggest that GATA6 simultaneously activates the transcription of genes required for growth (REG4) and clonogenicity (LGR5), and the miR-363-GATA6-REG4/LGR5 pathway is critical for colorectal tumorigenesis. HT29 cells were transfected with a siRNA targeting LGR5.

2016-06-15 | E-GEOD-62317 | biostudies-arrayexpress

RNA-seq of LGR5(+) and LGR5(-) cells isolated from human colon adenoma organoids

Project description:RNA-seq of LGR5(+) and LGR5(-) cells isolated from human colon adenoma organoids

| PRJEB14077 | ENA

Expression data from xenograft tumors derived from LoVo colon cancer lines +/- constitutive LIN28B expression

2010-12-29 | GSE26335 | GEO