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Analysis of differential gene expression in Regorafenib resistant human HCC cells either expressing or lacking Axl

ABSTRACT: Analysis of differential gene expression in Regorafenib resistant human HCC cells either expressing or lacking Axl

PROVIDER: PRJNA982682 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24893767.fastq.gz	Fastqsanger.gz
	SRR24893768.fastq.gz	Fastqsanger.gz
	SRR24893769.fastq.gz	Fastqsanger.gz
	SRR24893770.fastq.gz	Fastqsanger.gz
	SRR24893771.fastq.gz	Fastqsanger.gz

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Analysis of differential gene expression in Regorafenib resistant human HCC cells either expressing or lacking Axl

Project description:Human HCC cell line SNU449 and SNU449-Axl-KO were cultured in increasing concentrations of Regorafenib (Rego) to generate resistance. Treatment naive cells (SNU449-ctrl and SNU449-Axl-KO-ctrl) and resistant ones (SNU449-Rego and SNU449-Axl-KO-Rego) were sent for RNA-seq.

2023-09-01 | GSE234647 | GEO

Effect of Gas6/Axl on HCC cell line gene expression

Project description:We adressed the impact of the receptor tyrosine kinase Axl and ist ligand Gas6 on gene expression in cellular HCC models, including cells harbouring Axl KO and exogenous reexpression.

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Effect of Gas6/Axl on HCC cell line gene expression

Project description:Effect of Gas6/Axl on HCC cell line gene expression

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Transcriptomic changes induced by regorafenib in sorafenib-resistant hepatocellular carcinoma cells: role of TGF-beta signaling and lncRNAs

Project description:We comprehensively analyzed the differentially expressed mRNAs (DEmRNAs) and lncRNAs (DElncRNAs) underlying the antitumor functions of regorafenib of sorafenib-resistant HCC cells using RNA sequencing (RNA-Seq). The treatment with regorafenib has demonstrated the ability to reverse the expression of genes and long non-coding RNAs (lncRNAs) that play crucial roles in signal pathways and epigenetic processes.

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Role of regorafenib in macrophage

Project description:Regorafenib increased M1/M2 ratio of BMDMs polarization and proliferation/activation of co-cultured T cells in vitro, indicating angiogenesis-independent immunomodulatory effects. Suppression of p38 kinase phosphorylation and downstream CREB-KLF4 activity in BMDMs by regorafenib reversed M2 polarization. Regorafenib enhanced antitumor efficacy of adoptively transferred antigen-specific T cells, whereas macrophage deletion negated regorafenib’s antitumor effects. Synergistic antitumor efficacy between low-dose regorafenib and anti-PD1 was associated with multiple immune-related pathways in the tumor microenvironment.

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Gene expression analysis of dissociated and FDG FACS-sorted mammary glands of 16 week old nulliparous AXL +/LacZ and AXL LacZ/LacZ mice (B6.129P2-AXLtm1Dgen strain, Jackson Labs)

Project description:The receptor tyrosine kinase AXL is associated with epithelial plasticity in several solid tumors including breast cancer and AXL-targeting agents are currently in clinical trials. We hypothesized that AXL is a driver of stemness traits in cancer by co-option of a regulatory function normally reserved for stem cells. AXL-expressing cells in human mammary epithelial ducts co-expressed markers associated with multipotency, and AXL inhibition abolished colony-formation and self-maintenance activities while promoting terminal differentiation in vitro. Axl-null mice did not exhibit a strong developmental phenotype, but enrichment of Axl+ cells was required for mouse mammary gland reconstitution upon transplantation, and Axl-null mice had reduced incidence of Wnt1-driven mammary tumors. An AXL-dependent gene signature is a feature of transcriptomes in basal breast cancers, and reduced patient survival irrespective of subtype. Our interpretation is that AXL regulates access to epithelial plasticity programs in MaSCs and, when coopted, maintains acquired stemness in breast cancer cells.

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Project description:Low-dose regorafenib (5 mg/kg/day, corresponding to about half of human clinical dosage) inhibited tumor growth and angiogenesis in vivo similarly to DC-101 (anti-VEGFR antibody) but produced higher T cell activation and M1 macrophage polarization, Regorafenib increased M1/M2 ratio of BMDMs polarization and proliferation/activation of co-cultured T cells in vitro, indicating angiogenesis-independent immunomodulatory effects. Suppression of p38 kinase phosphorylation and downstream CREB-KLF4 activity in BMDMs by regorafenib reversed M2 polarization. Regorafenib enhanced antitumor efficacy of adoptively transferred antigen-specific T cells, whereas macrophage deletion negated regorafenib’s antitumor effects. Synergistic antitumor efficacy between low-dose regorafenib and anti-PD1 was associated with multiple immune-related pathways in the tumor microenvironment.

2021-01-27 | GSE148947 | GEO

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Project description:We report the comparative investigation of gene expression profiles between genetic inactivation AXL cell and AXL wild type cells in two independent We found a list of AXL signaling target genes that are important for tumor invasion and angiogenesis.

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Expression data from cholangiocarcinoma cell lines and regorafenib treatment.

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Gas6/Axl signaling activates Akt in liver cancer cells

Project description:We investigated which signaling pathways downstream of Gas6/Axl promote the invasive phenotype of liver cancer cells. Thus, we performed phospho-proteomic analysis of MR hepatocytes and those expressing Axl (MR-Axl) in the presence and absence of Gas6. Protein-clustering based on the pattern of phosphorylation across the conditions and samples revealed four clusters: phospho-sites that are upregulated dependent on Axl expression (cluster 1) or Gas6 expression (cluster 2) and phospho-sites that are downregulated dependent on Axl expression (cluster 3) or Gas6 expression (cluster 4). Functional enrichment analysis showed enrichment of protein sets associated with cellular polarity and motility depending on changes in Axl expression and Gas6 activation. Furthermore, we analyzed phospho-proteomic data to estimate the activity of kinases based on kinase-substrate interactions using PhosR. Kinase perturbation analysis indicated mammalian target of rapamycin (mTOR) as the one with the highest upregulated activity in Gas6-stimulated MR-Axl cells compared to Gas6-stimulated MR cells. Accordingly, we analyzed substrates of mTOR and found that phosphorylation of Akt1 (Ser473) was upregulated in cluster 1 and highly increased in Gas6-stimulated MR-Axl, suggesting that Akt is regulated by Axl.

2024-05-23 | PXD047577 | Pride

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