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NCOA5 knockout suppresses epithelial-to-mesenchymal transition (EMT) impairing cell proliferation and migration in Hepatocellular Carcinoma cells

ABSTRACT: NCOA5 knockout suppresses epithelial-to-mesenchymal transition (EMT) impairing cell proliferation and migration in Hepatocellular Carcinoma cells

PROVIDER: PRJNA438307 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6834145_1.fastq.gz	Fastqsanger.gz
	SRR6834145_2.fastq.gz	Fastqsanger.gz
	SRR6834146_1.fastq.gz	Fastqsanger.gz
	SRR6834146_2.fastq.gz	Fastqsanger.gz

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NCOA5 knockout suppresses epithelial-to-mesenchymal transition (EMT) impairing cell proliferation and migration in Hepatocellular Carcinoma cells

Project description:Nuclear receptor coactivator 5 (NCOA5) is an AF2-independent coactivator that contains both transcriptional activation and repression domains. Previous studies have shown that NCOA5 plays an important role in the development of a variety of malignancies. However, the underlying mechanisms remain unclear. In our study, we successfully generated the NCOA5 knockout liver cancer cell lines by CRISPR/Cas9 -mediated genome editing and found that NCOA5 knockout inhibited the proliferation and migration of hepatocellular carcinoma (HCC) cells significantly, meanwhile led to a marked decrease in tumor microsphere formation. Furthermore, mechanistic analyses indicated that NCOA5 knockout can inhibit the EMT process. In this study, knocking out NCOA5 in hepatoma cells LM3 with CRISPR/Cas9 provides an important cellular model for studying role of NCOA5 in HCC. In conclusion , Oour study provides new insights and evidence that NOCA5 was significantly correlated with the progression of HCC and was particularly involved in EMT.

2019-05-21 | GSE111829 | GEO

SMS2 suppresses hepatocellular carcinogenesis by impairing p85/p110 interaction

Project description:SMS2 suppresses hepatocellular carcinogenesis by impairing p85/p110 interaction

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SAMD1 suppresses epithelial-mesenchymal transition (EMT) in pancreatic ductal adenocarcinoma.

Project description:SAMD1, a CpG island-binding protein, plays a pivotal role in the repression of its target genes by influencing the activity of KDM1A. Despite its significant correlation with outcomes in various tumor types, SAMD1's role in cancer has remained largely unexplored. In this study, we focus on pancreatic ductal adenocarcinoma (PDAC) and reveal that SAMD1 is a repressor of genes associated with epithelial-mesenchymal transition (EMT). Upon depletion of SAMD1 in PDAC cells, we observed significantly increased migration rates. Furthermore, high SAMD1 expression in PDAC patients correlated with lower expression of EMT signature genes and better prognosis, further underscoring its suppressive role. In-depth analysis revealed that SAMD1 exerts its effects by binding to specific genomic targets, including CDH2, encoding N-Cadherin, which emerged as a driver of enhanced migration upon SAMD1 knockout. Our investigations further demonstrated reduced chromatin-binding activity of SAMD1 in PDAC cells, prompting a search for regulatory mechanisms. This led to the discovery of the FBXO11-containing E3 ubiquitin ligase complex as a novel interactor of SAMD1, critically influencing its chromatin binding genome-wide. High FBXO11 expression in PDAC is associated with poor prognosis and increased expression of EMT-related genes, implying an antagonistic relationship between SAMD1 and FBXO11. In summary, our findings provide new insights into the regulation of EMT-related genes in PDAC, shedding light on the intricate role of SAMD1 and its interplay with FBXO11 in this particular cancer type.

2024-07-12 | PXD044104 | Pride

LncRNA SNHG5 suppresses cell migration and invasion of human lung adenocarcinoma via regulation of epithelial-mesenchymal transition

Project description:Long noncoding RNAs (lncRNAs) are emerging as important regulators in cellular processes. In the present study, the effects of the long non-coding RNA, SNHG5 was investigated in lung adenocarcinoma (LAD) and we also revealed the underlying mechanisms of it. Overexpressed SNHG5 suppressed migration and invasion of LAD cell line A549 in vitro. Transcriptome sequencing analysis supported the inhibitory effects of SNHG5 were associated with cell adhesion molecules. In addition, western blot and immunofluorescence showed that the expression of SNHG5 was associated with epithelial-mesenchymal transition (EMT) markers. Furthermore, we determined the effects of SNHG5 in EMT procession of A549 induced by TGF-β1. Consistent with previous results, overexpression of SNHG5 suppressed the migration and invasion, and also the expression of EMT-related transcription factors including Snail, SLUG and ZEB1 in EMT of A549 reduced by TGF-β1. Moreover, qRT-PCR demonstrated expression of SNHG5 was positively correlated with E-cadherin protein expression, but negatively correlated with N-cadherin and Vimentin in LAD tissues. In summary, our study demonstrated that lncRNA SNHG5 could suppress cell migration and invasion of LAD cancer by inhibiting EMT procession, highlighting the potential of SNHG5 as a therapy strategy for lung adenocarcinoma.

2020-01-17 | GSE143766 | GEO

Identifying molecular mechanisms of neural crest (NC) EMT and cell migration

Project description:Purpose: To identify differntially expressed transcripts in TP-0903 treated embryos that impair cranila NC EMT and cell migration in zebrafish embryos Methods: zebrafish embryos treated at 13 hpf with 5-7uM TP-0903 and DMSO for 1-, 4- and 8-hrs at 28Â°C. 35 embryos were collected for each treatment. Results: TP-0903 increases expression of several retinoic acid target genes including genes from within the retinoid pathway Conclusions: TP-0903 causes a direct increase in RA signaling that impairs cranial NC EMT and cell migration in zebrafihs embryos mRNA profiles of zebrafish embryos treated with TP-0903 and DMSO were generated by RNA-Seq, in quadruplicates, using Illumina Hi Seq

2016-02-18 | E-GEOD-72322 | biostudies-arrayexpress

HTR1D inhibitor GR127935 suppresses proliferation and migration of gastric cancer via cell cycle arrest and repression of EMT

Project description:HTR1D inhibitor GR127935 suppresses proliferation and migration of gastric cancer via cell cycle arrest and repression of EMT

| PRJNA825544 | ENA

Identifying molecular mechanisms of neural crest (NC) EMT and cell migration

Project description:Purpose: To identify differntially expressed transcripts in TP-0903 treated embryos that impair cranila NC EMT and cell migration in zebrafish embryos Methods: zebrafish embryos treated at 13 hpf with 5-7uM TP-0903 and DMSO for 1-, 4- and 8-hrs at 28°C. 35 embryos were collected for each treatment. Results: TP-0903 increases expression of several retinoic acid target genes including genes from within the retinoid pathway Conclusions: TP-0903 causes a direct increase in RA signaling that impairs cranial NC EMT and cell migration in zebrafihs embryos

2016-02-18 | GSE72322 | GEO

EGF Induces Migration Independent of EMT or Invasion in A549 Lung Adenocarcinoma Cells

Project description:Tumors and tumor surrounding tissues produce multiple growth factors that influence tumor cell behavior via different signal transduction pathways. Growth factors like transforming growth factor beta (TGFβ) and epidermal growth factor (EGF) were shown to induce proliferation, migration and invasion in different cell models. Both factors are frequently overexpressed in cancer and will often act in combination. Although both factors are being used as rational targets in clinical oncology, similarities and differences of their contributions to cancer cell migration and invasion are not fully understood. Here we compared the impact of TGFβ, EGF and the combination of both factors on A549 cells. Both factors stimulated A549 migration to a similar extent but with a different kinetic and the combination had an additive effect. While EGF-induced migration depended on activation of the mitogen-activated protein kinase (MAPK) pathway, this pathway was dispensable for TGFβ-induced migration despite a strong activation by TGFβ. Proteome analysis revealed an overlap in expression patterns of migration-related proteins and associated gene ontology (GO) terms by TGFβ and EGF but only TGFβ induced the expression of epithelial to mesenchymal transition (EMT)-related proteins like matrix metalloproteinase 2 (MMP2). EGF in contrast, made no major contribution to EMT marker expression on either the protein or the transcript level. In line with these expression patterns, EGF was unable to increase invasion of A549 cells on its own and failed to enhance TGFβ-induced invasion. Overall, these data suggest that TGFβ and EGF may partly compensate each other for stimulation of cell migration but abrogation of TGFβ signaling may be more suitable for antagonizing invasion.

2021-04-08 | PXD023024 | Pride

The E3 ubiquitin ligase HectD1 suppresses EMT and metastasis by targeting the +TIP protein ACF7 for degradation

Project description:Cancer cells exploit the epithelial-to-mesenchymal transition (EMT) program toward metastasis. Cytoskeletal regulators are dually required in mesenchymal cells by promoting EMT-induced migration and sustaining the EMT program itself. In search for novel regulators of metastasis, we conducted an shRNA screen targeting a class of microtubule regulators, the plus-end tracking proteins (+TIPs). We show that the +TIP ACF7 is required for both the maintenance of EMT and to promote migration. We identified HectD1 as a potent E3 ubiquitin ligase mediating ACF7 degradation. Depletion of HectD1 robustly increases ACF7 protein levels and this is sufficient to enhance migration and EMT in cells, as well as facilitate metastasis in vivo. Ours results report the HectD1/ACF7 axis as a novel regulator of metastasis of breast cancer cells.

2018-01-03 | GSE100092 | GEO

ZNF827-dependent splicing dynamics are critical for EMT during development and disease [RNA-seq]

Project description:Epithelial to mesenchymal transition (EMT) is a multi-step process during which epithelial cells become mesenchymal stem cells. EMT is involved during embryonic development, wound healing, fibrosis and tumor metastasis. Here we show that ZNF827, a C2H2-zinc finger containing protein, is critical for molecular and phenotypic changes underlying EMT. We demonstrate that ZNF827 depletion suppresses tumor metastasis and cortical neurogenesis in vivo by impairing EMT. Further analysis showed that ZNF827 is critical for global alternative splicing (AS) during EMT. We further reveal that ZNF827 interacts with various components of core splicing machinery and directly binds DNA. ZNF827 depletion leads to alteration of epigenetic landscape at its target genomic region which might be important for alternative splicing of these target genes. Our findings established ZNF827 as a novel regulator of AS during development and disease contexts of EMT.

2023-02-14 | GSE99720 | GEO

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