Mechanism of OGT-mediated FASN glycosylation regulating JNK/ICAM1 pathway in Liver cancer stem cell metastasis [Transwell]
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ABSTRACT:
PROVIDER: PRJNA1136504 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29847446.fastq.gz | Fastqsanger.gz | |||
| SRR29847446_1.fastq.gz | Fastqsanger.gz | |||
| SRR29847446_2.fastq.gz | Fastqsanger.gz | |||
| SRR29847447_1.fastq.gz | Fastqsanger.gz | |||
| SRR29847447_2.fastq.gz | Fastqsanger.gz |
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Project description:We performed transcriptome sequencing analysis on LCSCs with different metastatic abilities. KEGG enrichment showed that genes upregulated during LCSC3 metastasis were related to cell membrane pathways. qPCR and flow cytometry confirmed that FASN expression was significantly upregulated during LCSCs metastasis. ICAM1 affects EMT, invadopodia formation, migration and invasion ability of LCSCs. ICAM1 plays a key role in the process of liver metastasis and the development of hepatocellular carcinoma in mice. FASN is also highly expressed during LCSC metastasis. Silencing FASN reduces the expression level of stemness genes, migration and invasion ability, and self-renewal ability of LCSCs. GSEA analysis indicated that transcriptome sequencing results after FASN knockdown were mainly enriched in the EMT process. FASN affects the expression of ICAM1 through the JNK/c-Jun axis in the MAPK pathway, and OGT is involved in the glycosylation process of ICAM1 regulating FASN, thereby affecting the migration ability of LCSCs.
2024-11-11 | GSE272352 | GEO
Project description:We performed transcriptome sequencing analysis on LCSCs with different metastatic abilities. KEGG enrichment showed that genes upregulated during LCSC3 metastasis were related to cell membrane pathways. qPCR and flow cytometry confirmed that FASN expression was significantly upregulated during LCSCs metastasis. ICAM1 affects EMT, invadopodia formation, migration and invasion ability of LCSCs. ICAM1 plays a key role in the process of liver metastasis and the development of hepatocellular carcinoma in mice. FASN is also highly expressed during LCSC metastasis. Silencing FASN reduces the expression level of stemness genes, migration and invasion ability, and self-renewal ability of LCSCs. GSEA analysis indicated that transcriptome sequencing results after FASN knockdown were mainly enriched in the EMT process. FASN affects the expression of ICAM1 through the JNK/c-Jun axis in the MAPK pathway, and OGT is involved in the glycosylation process of ICAM1 regulating FASN, thereby affecting the migration ability of LCSCs.
2024-11-11 | GSE269783 | GEO
Project description:Mechanism of OGT-mediated FASN glycosylation regulating JNK/ICAM1 pathway in Liver cancer stem cell metastasis
| PRJNA1123685 | ENA
Project description:TET2 directly interacts with OGT, which is important for the chromatin association of OGT in vivo. Although this specific interaction does not regulate the enzymatic activity of TET2, it facilitates OGT-dependent histone O-GlcNAcylation. Moreover, OGT associates with TET2 at transcription starting sites (TSS). Down-regulation of TET2 reduces the amount of H2B S112 GlcNAc marks in vivo, which are associated with gene transcription regulation. We found that OGT interacts with TET2 tightly. Using ChIP-seq with specific antibodies, we tested the co-localization of TET2 and OGT in genome level.
2012-12-11 | E-GEOD-41720 | biostudies-arrayexpress
Project description:We examined FASN knockdown LNCaP cells obtained by shRNA transduction with Mission lentiviral transduction particles (SHCLNV-NM 00410, TRCN3128, Sigma) (FASN-RNAi cells). In this study, we used cells transfected with non-targeting shRNA as a control (control-RNAi cells). The expression of genes related to cellular proliferation (phospholipase A2, group IVA, PLA2G4A; tensin 3, TNS3; glypican 4 GPC4), cell adhesion and extracellular matrix organization [peroxidasin homolog (Drosophila) PXDN; sarcoglycan epsilon, SGCE; von Willebrand factor, VWF; hydroxysteroid (17-beta) dehydrogenase 12, HSD17B12; cysteine-rich secretory protein LCCL domain containing 2, CRISPLD2], and cell motility (TNS3, RAP2B member of RAS oncogene family, RAP2B) were shown to be down-regulated by FASN inhibition with RNAi. FASN inhibition led to down-regulation of the PLA2G4A and HSD17B12 genes encoding phospholipase A2 and 17-beta hydroxysteroid dehydrogenase, respectively, which are the key enzymes related to production of an intracellular second messenger arachidonic acid and androgen hormones, both playing roles in promotion of tumor progression. We also found that the genes related to arachidonic acid signalling, including RGS2, SPAG16, VWF and RAP2B, were also suppressed with FASN inhibition. Gene expression profiling therefore demonstrated that FASN inhibition induces down-regulation of genes related to cell proliferation, cell adhesion, migration, and invasion, as well as the production of arachidonic acid and androgen hormones, both of which drive tumor progression. Total RNA isolation was performed with a Micro-to-Midi total RNA purification system (Invitrogen). The integrity of total RNAs was evaluated using an Agilent 2100 Bioanalyzer (Agilent Technologies). Low Input Quick Amp Labeling Kit, one-color (Agilent Technologies) was used to prepare Cy3-labelled target cRNA according to the manufacturer's instructions. Labeled cRNAs were hybridized with a SurePrint G3 Human GE 8M-CM-^W60K Microarrays (Agilent Technologies). Two separate hybridizations were performed for each sample. Array images were captured using a DNA Microarray Scanner (Agilent Technologies), and data were analyzed using Feature Extraction Software (Agilent Technologies) to obtain background-corrected signal intensities. The data were further analysed with GeneSpring GX Software (Version 11.0, Agilent Technologies). After filtering of data, mRNAs differentially expressed in target versus control were considered using the Fisher exact test, followed by multiple corrections using the Benjamini and Hochberg false discovery rate (FDR) method. Gene sets with a FDR q-value < 0.05 were considered significant.
2012-07-09 | E-GEOD-39183 | biostudies-arrayexpress
Project description:The fatty acid synthase (FASN) is the major fat synthesizing enzyme. FASN is an indispensable enzyme because mice with genetic deletion of Fasn are not viable. Apart from its physiological function, previous studies indicated that FASN could also exert a pathophysiological role, in the heart, because patients with heart failure showed up-reguation of FASN. To investigate the in vivo function of FASN up-regulation in the heart, we generated mice with myocardium-specific expression of FASN under control of the alpha-MHC promoter. Two different founder lines were generated with high and low FASN over-expression. Microarray gene expression profiling of heart tissue was performed of heart tissue from transgenic mice with high and low FASN expression Microarray gene expression profiling was performed with heart tissue isolated from three study groups: (i) Transgenic mice with high cardiac FASN expression, (ii) transgenic mice with low cardiac FASN expression, and (iii) B6 control mice.
2013-07-31 | E-GEOD-49351 | biostudies-arrayexpress
Project description:TET2 directly interacts with OGT, which is important for the chromatin association of OGT in vivo. Although this specific interaction does not regulate the enzymatic activity of TET2, it facilitates OGT-dependent histone O-GlcNAcylation. Moreover, OGT associates with TET2 at transcription starting sites (TSS). Down-regulation of TET2 reduces the amount of H2B S112 GlcNAc marks in vivo, which are associated with gene transcription regulation.
2012-12-11 | GSE41720 | GEO
Project description:O-linked N-acetylglucosamine (O-GlcNAc ) transferase (OGT) activity is essential for embryonic stem (ES) cell viability and mouse development. OGT is present in both cytoplasm and nucleus of different cell types and mediates serine or threonine glycosylation. The Ogt gene locus resides on the X-chromosome and its activity is required for the viability of male ES cells. Using Ogt conditional knock out (KO) ES cells it was shown the failure of establishing stable KO ES clones further suggesting that Ogt activity is required for ES cell self-renewal and pluripotency. For understanding these changes, we performed global gene expression upon silencing of Ogt mediated by esiRNA in mouse Embryonic Stem Cells. Total RNA was extracted from E14 ES cells (derived from Ola129 mice) transiently transfected with Ogt specific and control esiRNA oligos 48 hrs. post-transfection.
2013-01-06 | E-GEOD-39321 | biostudies-arrayexpress
Project description:These data include the genome wide location analysis of Ogt by ChIP of Ogt in mouse ES cells. Precipitation of formaldehyde cross-linked chromatin prepared from mouse ES cell using specific antibody against OGT and IgG as control.
2013-01-06 | E-GEOD-39154 | biostudies-arrayexpress
Project description:We examined FASN knockdown LNCaP cells obtained by shRNA transduction with Mission lentiviral transduction particles (SHCLNV-NM 00410, TRCN3128, Sigma) (FASN-RNAi cells). In this study, we used cells transfected with non-targeting shRNA as a control (control-RNAi cells). The expression of genes related to cellular proliferation (phospholipase A2, group IVA, PLA2G4A; tensin 3, TNS3; glypican 4 GPC4), cell adhesion and extracellular matrix organization [peroxidasin homolog (Drosophila) PXDN; sarcoglycan epsilon, SGCE; von Willebrand factor, VWF; hydroxysteroid (17-beta) dehydrogenase 12, HSD17B12; cysteine-rich secretory protein LCCL domain containing 2, CRISPLD2], and cell motility (TNS3, RAP2B member of RAS oncogene family, RAP2B) were shown to be down-regulated by FASN inhibition with RNAi. FASN inhibition led to down-regulation of the PLA2G4A and HSD17B12 genes encoding phospholipase A2 and 17-beta hydroxysteroid dehydrogenase, respectively, which are the key enzymes related to production of an intracellular second messenger arachidonic acid and androgen hormones, both playing roles in promotion of tumor progression. We also found that the genes related to arachidonic acid signalling, including RGS2, SPAG16, VWF and RAP2B, were also suppressed with FASN inhibition. Gene expression profiling therefore demonstrated that FASN inhibition induces down-regulation of genes related to cell proliferation, cell adhesion, migration, and invasion, as well as the production of arachidonic acid and androgen hormones, both of which drive tumor progression.
2012-07-10 | GSE39183 | GEO