Project description:Fetal-maternal immune tolerance guarantees a successful pregnancy throughout gestation. HLA-G, a non-classical human leukocyte antigen (HLA) molecule exclusively expressed in extravillous trophoblasts (EVT), is a crucial factor in establishing fetal-maternal immune tolerance by interacting with inhibitory receptors on various maternal immune cells residing in the uterus. While trophoblast specific Cis-Regulatory Elements (CREs) impacting HLA-G transcription have been described, the identity of trans-acting factors controlling HLA-G expression in EVT remains poorly understood. Utilizing a genome-wide CRISPR-Cas9 knockout screen, we find that the WNT signaling pathway negatively regulates HLA-G expression in EVT. APC is a key component of the destruction complex for cytoplasmic β-catenin, switching off the canonical WNT pathway. This dataset containes the transcriptomics in JEG-3 cells upon APC knockout.
Project description:IL-11 increases the invasiveness of JEG-3 cells while, reduces the invasiveness of HTR-8/SVneo cells. This study examines the effect of IL-11 on gene expression in trophobalstic cell models viz. JEG-3 and HTR-8/SVneo cells to resolve the controversies associated with the IL-11 mediated regulation of the invasiveness of these two cell lines.
Project description:Both leukemia inhibitory factor (LIF) and interleukin-6 (IL-6) increase the invasiveness of JEG-3 and HTR-8/SVneo cells. This study examines the effect of LIF and IL-6 on gene expression in trophoblastic cell models viz. JEG-3 and HTR-8/SVneo cells to decipher the molecular basis of the increase in invasiveness.
Project description:IL-11 increases the invasiveness of JEG-3 cells while, reduces the invasiveness of HTR-8/SVneo cells. This study examines the effect of IL-11 on gene expression in trophobalstic cell models viz. JEG-3 and HTR-8/SVneo cells to resolve the controversies associated with the IL-11 mediated regulation of the invasiveness of these two cell lines. JEG-3 and HTR-8/Svneo cells were stimulated with IL-11 (200 ng/ml) for 24 h in pain medium keeping un-treated cells as control. After 24 h of stimulation, total RNA was isolated from these cells and used for the microarray experiments. These experiments were performed once.
Project description:Both leukemia inhibitory factor (LIF) and interleukin-6 (IL-6) increase the invasiveness of JEG-3 and HTR-8/SVneo cells. This study examines the effect of LIF and IL-6 on gene expression in trophoblastic cell models viz. JEG-3 and HTR-8/SVneo cells to decipher the molecular basis of the increase in invasiveness. JEG-3 and HTR-8/Svneo cells were stimulated with LIF (50 ng/ml) and IL-6 (100 ng/ml) for 24 h in plain medium keeping untreated cells as a control. After 24 h of stimulation, total RNA was isolated from these cells and used for microarray experiments. These experiments were performed once.
Project description:To investigate effect of WNT hyperactivation by CTNNB1 overexpression or APC knockdown on gene expression and probe possible mechanism of cell viability effect, we overexpressed GFP/CTNNB1, or induce knockdown of APC by shNT1 (non-targeting) and shAPC
Project description:The first step in the development of human colorectal cancer is the aberrant hyperactivation of the Wnt signaling pathway, predominantly caused by inactivating mutations in the adenomatous polyposis coli (Apc) gene encoding an essential tumor suppressor. The gene encoding transcriptional factor msh homeobox 1 (Msx1) displayed robust upregulation upon Apc inactivation in intestinal epithelium isolated in mice harboring the conditional allele of the Apc gene. To identify the gene signature in the small intestine upon Msx1 depletion, small intestinal epithelium from mice harboring conditional alleles of Apc and Msx1 was isolated and the gene expression profile was compared with control mice harboring the conditional allele of Apc only.
Project description:The first step in the development of human colorectal cancer (CRC) is the aberrant hyperactivation of the Wnt signaling pathway, predominantly caused by inactivating mutations in the adenomatous polyposis coli (APC) gene which encodes an essential tumor suppressor. In order to identify genes affected by Apc loss, expression profiling of intestinal epithelium isolated from mice harboring the conditional allele of the gene was performed. The gene encoding transcriptional factor msh homeobox 1 (Msx1) displayed robust upregulation upon Apc inactivation. To characterize the gene signature in colon upon Msx1 depletion, colonic epithelium from mice harboring conditional alleles of Apc and Msx1 was isolated and the gene expression profile was compared with control mice harboring the conditional allele of Apc only.