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Mechanism of OGT-mediated FASN glycosylation regulating JNK/ICAM1 pathway in Liver cancer stem cell metastasis [Transwell]

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE272352 | GEO | 2024/11/11

REPOSITORIES: GEO

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Mechanism of OGT-mediated FASN glycosylation regulating JNK/ICAM1 pathway in Liver cancer stem cell metastasis

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

Mechanism of OGT-mediated FASN glycosylation regulating JNK/ICAM1 pathway in Liver cancer stem cell metastasis

Project description:Mechanism of OGT-mediated FASN glycosylation regulating JNK/ICAM1 pathway in Liver cancer stem cell metastasis

| PRJNA1123685 | ENA

Mechanism of OGT-mediated FASN glycosylation regulating JNK/ICAM1 pathway in Liver cancer stem cell metastasis [Transwell]

Project description:Mechanism of OGT-mediated FASN glycosylation regulating JNK/ICAM1 pathway in Liver cancer stem cell metastasis [Transwell]

| PRJNA1136504 | ENA

AK2 promotes the migration and invasion of lung adenocarcinoma by activating TGF-β/Smad pathway in vitro and in vivo

Project description:Adenylate kinase 2 (AK2) is a wide-spread and highly conserved protein kinase whose main function is to catalyze the exchange of nucleotide phosphate groups. In this study, we showed that AK2 regulated tumor cell metastasis in lung adenocarcinoma. Positive expression of AK2 is related to lung adenocarcinoma progression and poor survival of patients. Knockdown or knockout of AK2 inhibited, while overexpression of AK2 promoted, human lung adenocarcinoma cell migration and invasion ability. Differential proteomics results showed that AK2 might be closely related to epithelial-mesenchymal transition (EMT). Further research indicated that AK2 regulated EMT occurrence through the Smad-dependent classical signaling pathways as measured by western blot and qPCR assays. Additionally, in vivo experiments showed that AK2-knockout in human lung tumor cells reduced their EMT-like features and formed fewer metastatic nodules both in liver and in lung tissues. In conclusion, we uncover a cancer metastasis-promoting role for AK2 and provide a rationale for targeting AK2 as a potential therapeutic approach for lung cancer.

2021-09-18 | PXD028247 | Pride

Ruscone2023 - Logical model of Tumor Cell Invasion

Project description:This model builds upon two published models focused on the early steps of metastasis by Cohen et al. and on EMT process by Selvaggio et. al. The initial model of Cohen and colleagues was built with two inputs: the ECMenv, which monitored the status of the extracellular matrix, and DNA_damage, which considered DNA alterations that trigger death signals. Four additional inputs were added to account for the presence of Oxygen, growth factors (as GF), TGFbeta and the contact with other neighboring cells (as Neigh). The phenotypes, or outputs of the model include CellCycleArrest, Apoptosis, EMT, ECM_adh (for cell adhesion), ECM_degrad (for cell degradation), Cell_growth (for the dynamics of the tumor growth) and Cell_freeze (for cell motility ability). New genes and pathways include mechanisms around p63 and SRC. Genes from the Hippo pathway and RhoGTPases, such as YAP1, FAK and RAC1 were also inserted to link external signals (i.e., cell–cell contact, stiffness of the extracellular matrix, and stress signals) and intracellular regulation. The resulting network encompasses 45 nodes, with 6 input nodes, representing the possible interactions of an individual cell with external elements, and 8 output nodes or read-outs describing the possible observed phenotypes. This model was initially developed as a MaBoSS model for a multi-scale model of tumor invasion, developed with PhysiBoSS. As SBML-qual cannot describe fully a MaBoSS model yet, we also include the MaBoSS BND and CFG files.

2023-06-27 | MODEL2304070002 | BioModels

Epithelial-to-Mesenchymal Transition of Murine PTEN-/- Liver Tumor Cells Promotes Tumor Growth and Invasion

Project description:Background: Epithelial-to-Mesenchymal Transition (EMT) is predicted to play a critical role in tumor progression and metastasis in Hepatocellular Carcinoma. Our goal was to elucidate a mechanism of tumor proliferation and metastasis using a novel murine model of EMT. Methods: 2Ã106 liver cells isolated from Ptenloxp/loxp;Alb-Cre+ mice, expanded from a single CD133+CD45- cell clone, Passage 0 (P0), were sequentially transplanted to obtain two passages of tumor cells, Passage 1 and 2 (P1 & P2) . Cells were analyzed for gene expression using microarray and real-time PCR. Functional analysis included cell proliferation, migration, and invasion in-vitro and orthotopic tumor growth and metastasis assays in-vivo. Results: Although P0, P1, and P2 each formed tumors consistent with mixed liver epithelium, within the P2 cells, two distinct cell types were clearly visible: cells with epithelial morphology similar to the P0 cells, and cells with fibroblastoid morphology. The P2 mesenchymal cells demonstrated increased locomotion on wound healing, increased cell invasion on Matrigel basement membrane, increased EMT associated gene Snail1, Zeb1, and Zeb2 expression, and down-regulated E-cadherin. P2 mesenchymal cells demonstrated significantly faster tumor growth compared to P2 Epithelial counterparts, with peritoneal seeding and invasion of intestine, pancreas, spleen, and lymph nodes. Furthermore, P2 mesenchymal cells secreted high levels of Hepatocyte Growth Factor (HGF), which acted in paracrine fashion to drive epithelial cells to undergo EMT. Conclusion: EMT is associated with a high rate of liver tumor proliferation, invasion, and metastasis in-vivo, which is driven by HGF in a feed-forward mechanism. Total RNA isolated from subcutaneously transplanted tumors with PTENloxp/loxp;Alb-Cre+ genetic background

2010-05-28 | E-GEOD-18255 | biostudies-arrayexpress

Transcriptome of EMT induced MCF10A cells by TGFb treatment or SNAIL S6A expression.

Project description:EMT, Epithelial to mesenchymal transition is a developmental biology process associated with migration, known to be involved in cancer metastasis. To study this process, we used the breast epithelial cell line MCF10A that enter in EMT after treatment with the cytokine TGFB or by expression of EMT transcriptor factor SNAIL.

2017-01-30 | GSE89152 | GEO

RNF185 control of COL3A1 expression limits prostate cancer migration and metastatic potential.

Project description:RNF185 is a RING finger domain-containing ubiquitin ligase implicated in ER-associated degradation. Prostate tumor patient data analysis revealed a negative correlation between RNF185 expression and prostate cancer progression and metastasis. Likewise, several prostate cancer cell lines exhibited greater migration and invasion capabilities in culture upon RNF185 depletion. Subcutaneous inoculation of mouse prostate cancer MPC3 cells stably expressing shRNA against RNF185 into mice resulted in larger tumors and more frequent lung metastases.RNA-sequencing and Ingenuity Pathway Analysis identified wound healing and cellular movement among the most significant pathways upregulated in RNF185-depleted, compared to control prostate cancer cells. Gene Set Enrichment Analyses performed in samples from patients harboring low RNF185 expression and in RNF185-depleted lines confirmed the deregulation of genes implicated in EMT. Among those, COL3A1 was identified as the primary mediator of RNF185’s ability to impact migration phenotypes. Correspondingly, enhanced migration and metastasis of RNF185 KD prostate cancer cells were attenuated upon co-inhibition of COL3A1. Our results identify RNF185 as a gatekeeper of prostate cancer metastasis, partly via its control of COL3A1 availability.

2024-08-09 | PXD045473 | Pride

Prognostic signature of epithelial-mesenchymal transition in breast cancer

Project description:Epithelial-mesenchymal transition (EMT), a switch of polarized epithelial cells to a migratory, fibroblastoid phenotype, is considered a key process driving tumor cell invasiveness and metastasis. Using breast cancer cell lines as a model system, we sought to discover gene-expression signatures of EMT with clinical and mechanistic relevance. A supervised comparison of epithelial and mesenchymal breast cancer lines defined a 200-gene EMT signature that was prognostic across multiple breast cancer cohorts. Immunostaining of LYN, a top-ranked EMT signature gene and Src-family tyrosine kinase, was associated with significantly shorter overall survival (P=0.02), and correlated with the basal-like (“triple-negative”) phenotype. In mesenchymal breast cancer lines, RNAi-mediated knockdown of LYN inhibited cell migration and invasion, but not proliferation. Dasatinib, a dual-specificity tyrosine kinase inhibitor, also blocked invasion (but not proliferation) at nanomolar concentrations that inhibit LYN kinase activity, suggesting that LYN is a likely target and invasion a relevant endpoint for dasatinib therapy. Our findings define a prognostically-relevant EMT signature in breast cancer, and identify LYN as a mediator of invasion and possible new therapeutic target (and theranostic marker for dasatinib response), with particular relevance to clinically-aggressive basal-like breast cancer. Cell Line: cell line(epithelial-like/fibroblast-like/normal breast fibroblasts) Keywords: Logical Set Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. HEEBO oligonucleotide microarrays from the Stanford Functional Genomics Facility were used to perform gene expression profiling of 20 human breast cell lines, in comparison to a universal RNA reference. Expression data were analyzed by Significance Analysis of Microarrays to identify a 200-gene signature characteristic of EMT.

2010-04-11 | E-GEOD-13915 | biostudies-arrayexpress

CD44 regulates epigenetic plasticity by mediating iron endocytosis - part 1

Project description:The biological process termed Epithelial-to-Mesenchymal Transition (EMT) plays a central role in cancer cell invasion, metastasis, self-renewal and resistance to therapy. Here, we characterize using quantitative LC-MS/MS the global changes in proteins levels occurring during EMT induced by epidermal growth factor in breast cancer MDA-MB-468 cells.

2019-10-01 | PXD011447 | Pride

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