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Long noncoding RNA NKX2-1-AS1 inhibits cell migration and regulates cell-adhesion independent of NKX2-1 in human lung carcinoma cells

ABSTRACT: Long noncoding RNA NKX2-1-AS1 inhibits cell migration and regulates cell-adhesion independent of NKX2-1 in human lung carcinoma cells

PROVIDER: PRJNA413536 | ENA |

REPOSITORIES: ENA

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Long noncoding RNA NKX2-1-AS1 inhibits cell migration and regulates cell-adhesion independent of NKX2-1 in human lung carcinoma cells

Project description:The long noncoding RNA NKX2-1-AS1 is highly expressed in primary lung adenocarcinomas compared to squamous carcinomas, similar to its adjacent protein-coding gene NKX2-1, but its contribution to lung tumorigenesis is not well understood. In this study we knockdown NKX2-1-AS1 by siRNA transfection and analyze the effect on gene expression in the lung carcinoma H441 cell line.

2018-09-28 | GSE104691 | GEO

Long Noncoding RNA HNF1A-AS1 Regulates Proliferation and Migration in Esophageal Adenocarcinoma Cells

Project description:Objectives: Long non-coding RNAs (lncRNAs) have been shown to play important roles in the development and progression of cancer. However, functional lncRNAs and their downstream mechanisms are largely unknown in the molecular pathogenesis of esophageal adenocarcinoma (EAC) and its progression. Design: lncRNAs that are abnormally upregulated in EACs were identified by RNA-seq analysis, followed by quantitative RT-PCR (qRTPCR) validation using tissues from 31 EAC patients. Cell biological assays in combination with siRNA-mediated knockdown were performed in order to probe the functional relevance of these lncRNAs. Results: We discovered that a lncRNA, HNF1A-AS1, is markedly upregulated in human primary EACs relative to their corresponding normal esophageal tissues (mean fold change 7.2, p<0.01). We further discovered that HNF1A-AS1 knockdown significantly inhibited cell proliferation and anchorage independent growth, suppressed S-phase entry, and inhibited cell migration and invasion in multiple in vitro EAC models (p<0.05). A gene ontological analysis revealed that HNF1A-AS1 knockdown preferentially affected genes that are linked to assembly of chromatin and the nucleosome, a mechanism essential to cell cycle progression. The well-known cancer-related lncRNA, H19, was the gene most markedly inhibited by HNF1A-AS1 knockdown. Consistent to this finding, there was a significant positive correlation between HNF1A-AS1 and H19 expression in primary EACs (p<0.01). In order to identify novel oncogenic lncRNAs in esophageal adenocarcinogenesis, we carried out RNA-seq of a matched NE-BE-EAC tissue pair

2013-10-21 | E-GEOD-48240 | biostudies-arrayexpress

LncRNA ITGB8-AS1 functions as a ceRNA to promote colorectal cancer growth and migration through integrin-mediated focal adhesion signaling

Project description:ITGB8-AS1 functions as a ceRNA to regulate cell proliferation and tumor growth of colorectal cancer (CRC) via regulating focal adhesion signaling. Targeting ITGB8-AS1 is effective in suppressing CRC cell growth and tumor growth. Elevated plasma levels of ITGB8-AS1 was detected in advanced-stage CRC. Thus, ITGB8-AS1 could serve as a potential therapeutic target and circulating biomarker in CRC.

2023-11-28 | GSE162297 | GEO

Long Noncoding RNA HNF1A-AS1 Regulates Proliferation and Migration in Esophageal Adenocarcinoma Cells

2013-10-21 | GSE48240 | GEO

Homeobox protein NKX2-3 modulates lymphocyte dynamics and promotes B-cell lymphomagenesis

Project description:Molecular cloning of a t(10;14)(q24;q32) from a B-cell lymphoma showed a recurrent breakpoint in homeobox NKX2-3 gene, which was highly expressed in comparison to non-expressing mature B lymphocytes. Epigenetically-mediated NKX2-3 over-expression was selectively found in patients with splenic marginal-zone lymphoma, MALT lymphoma and extranodal diffuse large-cell lymphoma. In young mice, restricted expression of NKX2-3 to lymphocytes activated multiple integrins (LFA-1, VLA-4, MAC-1), adhesion molecules (ICAM-1, MadCAM-1, L-selectin) and the chemokine receptor CXCR4 that enhanced their homing and migration to splenic tissues, whereby they were retained, progressively accumulating to form non-clonal tumors. At 18 months, B cells acquired genomic rearrangements and generated clonal B-cell lymphomas mirroring the spectrum of human NKX2-3-expressing tumors. Mouse and human lymphomas displaying NKX2-3 expression shared histopahological, genomic and molecular features, including canonical NF-KB activation. NF-KB inhibition reduced tumorigenecity of NKX2-3-positive lymphomas. Our study reveals that oncogenic NKX2-3 promotes B-cell lymphomagenesis by disturbing lymphocyte dynamics. Comparisson of global gene expression profiling between Emu-NKX2-3 transgenes mice and wild type mice.

2016-07-22 | E-GEOD-49356 | biostudies-arrayexpress

Homeobox protein NKX2-3 modulates lymphocyte dynamics and promotes B-cell lymphomagenesis

2016-07-22 | GSE49356 | GEO

LncRNA ITGB8-AS1 functions as a ceRNA to promote colorectal cancer growth and migration through integrin-mediated focal adhesion signaling

Project description:LncRNA ITGB8-AS1 functions as a ceRNA to promote colorectal cancer growth and migration through integrin-mediated focal adhesion signaling

| PRJNA681322 | ENA

Mammalian Pumilio Proteins Control Cellular Morphology, Migration, and Adhesion

Project description:Mammalian Pumilio Proteins Control Cellular Morphology, Migration, and Adhesion

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G3BP1 Ribonucleoprotein Complexes Regulate Focal Adhesion Protein Mobility and Cell Migration

Project description:G3BP1 Ribonucleoprotein Complexes Regulate Focal Adhesion Protein Mobility and Cell Migration

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Histone Methyltransferase Ezh2 Controls Cell Adhesion and Migration through Direct Methylation of the Extra-Nuclear Protein-Talin

Project description:Previously, we suggested a cytosolic role for the histone-methyltransferase Ezh2 in regulating lymphocyte activation, but molecular mechanisms underpinning this extra-nuclear function remained unclear. Here we show that Ezh2 regulates integrin-signaling and adhesion dynamics of neutrophils and dendritic cells. Ezh2 deficiency impaired integrin-dependent transendothelial migration of innate leukocytes and restricted disease progression in an animal model of multiple sclerosis. Direct methylation of talin, a key regulatory molecule in cell migration, by Ezh2 disrupted talin binding to F-actin and thereby promoted adhesion structure turnover. This regulatory effect was abolished by targeted disruption of Ezh2 interactions with Vav1. Our studies reveal a novel extra-nuclear function for Ezh2 in regulating adhesion dynamics with implications for leukocyte migration, immune responses and potentially pathogenic processes. Control and Ezh2-deficient bone marrow derived immature and mature dendritic cells were analyzed in triplicates

2015-03-09 | E-GEOD-60146 | biostudies-arrayexpress

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