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LRH1 silencing inhibits human colon cancer growth.

ABSTRACT: This study was undertaken to better determine the function of LRH-1 (NR5A2) in the colorectal cancers (CRC) through inducible shRNA-mediated knockdown within well-established CRC cell line Caco-2 Our work is the first to demonstrate that silencing of LRH-1 in established human CRC cell lines impairs proliferation though G0/G1 phase prolongation, and alteration in diverse cellular pathways consistent with the critical role of LRH-1 in CRC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE64695 | GEO | 2015/02/24

SECONDARY ACCESSION(S): PRJNA271662

REPOSITORIES: GEO

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LRH1 silencing inhibits human colon cancer growth.

Project description:This study was undertaken to better determine the function of LRH-1 (NR5A2) in the colorectal cancers (CRC) through inducible shRNA-mediated knockdown within well-established CRC cell line Caco-2 Our work is the first to demonstrate that silencing of LRH-1 in established human CRC cell lines impairs proliferation though G0/G1 phase prolongation, and alteration in diverse cellular pathways consistent with the critical role of LRH-1 in CRC. Two separate DNA sequences targeting the LRH-1 LBD- were cloned into parent vector pTripZ RHS4696 (Open Biosystems), with incorporation of silencing vector confirmed by fluorescent assay for marker TurboRFP. Non-silencing control cell lines were produced similarly using manufacturerM-bM-^@M-^Ys vector (Open Biosystems, RHS4743). Cells were plated at a concentration of 100,000 cells per ml in 12 well plates and allowed to attach overnight. shRNA expression was induced by the addition of 5 M-NM-<g/ml of doxycycline when the cells approached 75% confluence. Cells were harvested at 96 hours post induction using Trizol reagent (Life Technologies), and Total RNA harvested using PureLink RNA Mini Kit (Ambion) according to the manufacturerM-bM-^@M-^Ys protocol.

2015-02-24 | E-GEOD-64695 | biostudies-arrayexpress

LRH-1 Mitigates Intestinal Inflammatory Disease by Maintaining Epithelial Homeostasis and Cell Survival

Project description:We report the gene expression changes in murine small intestinal organoids following deletion of LRH-1 (NR5A2) and humanization by expression of human LRH-1 in mouse LRH-1 knockout organoids.

2018-07-04 | GSE116563 | GEO

Identification of Liver Receptor Homologue-1 (LRH-1)-regulated genes in HT29 colorectal cancer cells

Project description:Liver receptor homologue 1 (LRH-1) is an orphan nuclear receptor which has been implicated in the growth and development of breast, pancreatic and colorectal cancers (CRC). In order to identify novel LRH-1-regulated genes in CRC cells, we performed gene expression profiling following siRNA-mediated LRH-1 silencing in the CRC cell line HT29.

2015-10-01 | GSE65814 | GEO

Identification of Liver Receptor Homologue-1 (LRH-1)-regulated genes in HCT116 colorectal cancer cells

2015-10-01 | GSE65813 | GEO

Genome-wide mapping of Nr5a2 in mouse embryonic stem cells

Project description:Nr5a2 (also known as liver receptor homolog-1, Lrh-1) has been shown to bind both the proximal enhancer and proximal promoter regions of Pou5f1 and regulate Pou5f1 in the epiblast stage of mouse embryonic development (Gu et al., 2005). Nr5a2-null embryos display a loss of Oct4 expression in the epiblasts (Gu et al., 2005) and die between E6.5 and E7.5 (Gu et al., 2005; Pare et al., 2004). To identify the targets of Nr5a2, we generated a stable ES cell-line that expresses HA-tagged Nr5a2. Anti-HA antibody was used to immunoprecipitate HA-Nr5a2 for ChIP-seq analysis. Keywords: Transcription factor binding sites To identify the binding sites of Nr5a2, we generated a stable ES cell-line that expresses HA-tagged Nr5a2. Anti-HA antibody was used to immunoprecipitate HA-Nr5a2.

2010-01-22 | E-GEOD-19019 | biostudies-arrayexpress

A Role for Orphan Nuclear Receptor Liver Receptor Homolog-1 (LRH-1, NR5A2) in Primordial Follicle Activation

Project description:The ovarian reserve of follicles comprises all oocytes for lifetime fertility and is depleted by progressive activation. The orphan nuclear receptor liver receptor homolog 1 (LRH-1; Nr5a2) is essential for ovulation, but its role in the early stages of follicular development is not known. We therefore developed a model of conditional depletion of LRH-1 from early postnatal ovaries (postnatal day 4) and performed RNAsequencing to identify LRH-1 regulated genes during the earliest stages of follicular activation.

2022-10-24 | GSE216392 | GEO

Genome-wide mapping of Nr5a2 in mouse embryonic stem cells

2010-01-22 | GSE19019 | GEO

Expression data of NIH3T3 in G0 and G1 phases

Project description:NIH3T3 in the middle of G0 to G1 transion consists of the cells which is still staying G0 phase and the cells which enters G1. Monitoring the expressions of p27 and Cdt1 enables to distinguish these two; p27+/Cdt1+ cells as the cells in G0 phase and p27-Cdt1+ cells as G1 phase We sorted p27+Cdt1+ (G0) NIH3T3 cells and p27-Cdt1+ (G1) NIH3T3 cells in the middle of G0-G1 transition, 5 hours after serum addition following the serum addition using mVenus-p27K- and mCherry-hCdt1(30/120) . We compared the expression profiles of these NIH3T3 cells in G0 and G1 phases and identified the genes upregulated in G0 or G1 phases.

2014-02-21 | GSE46511 | GEO

Expression data of NIH3T3 in G0 and G1 phases

2014-02-21 | E-GEOD-46511 | biostudies-arrayexpress

Coiled-Coil Domain-Containing 68 Downregulation Promotes Colorectal Cancer Cell Growth by Inhibiting ITCH-Mediated CDK4 Degradation

Project description:Coiled-coil domain-containing 68 (CCDC68) plays different roles in cancer and is predicted as a tumor suppressor in human colorectal cancer (CRC). However, the specific role of CCDC68 in CRC and the underlying mechanisms remain unknown. Here, we showed that CCDC68 expression was lower in CRC than in corresponding normal tissues, and CCDC68 level was positively correlated with disease-free survival. Ectopic expression of CCDC68 decreased CRC cell proliferation in vitro and suppressed the growth of CRC xenograft tumors in vivo. CCDC68 caused G0/G1 cell cycle arrest, downregulated CDK4, and upregulated ITCH, the E3 ubiquitin ligase responsible for CDK4 protein degradation. This increased CDK4 degradation, which decreased CDK4 protein levels and inhibited CRC tumor growth. Collectively, the present results identify a novel CDK4 regulatory axis consisting of CCDC68 and ITCH, which suggest that CCDC68 is a promising target for the treatment of CRC.

2021-04-14 | PXD024343 | Pride

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