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Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and Stk11-/- Endothelial cell Transcriptomes [LKB1]

ABSTRACT: Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and Stk11-/- Endothelial cell Transcriptomes [LKB1]

PROVIDER: PRJNA765395 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16016207_1.fastq.gz	Fastqsanger.gz
	SRR16016207_2.fastq.gz	Fastqsanger.gz
	SRR16016208_1.fastq.gz	Fastqsanger.gz
	SRR16016208_2.fastq.gz	Fastqsanger.gz
	SRR16016209_1.fastq.gz	Fastqsanger.gz

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LKB1/STK11 Inactivation Leads to Expansion of Pro-Metastatic Tumor Sub-Population in Melanoma

Project description:Germline mutations in LKB1 (STK11) are associated with the Peutz–Jeghers syndrome (PJS), which includes aberrant mucocutaneous pigmentation, and somatic LKB1 mutations occur in 10% of cutaneous melanoma. By somatically inactivating Lkb1 with K-Ras activation (+/- p53 loss) in murine melanocytes, we observed variably pigmented and highly metastatic melanoma with 100% penetrance. LKB1 deficiency resulted in increased phosphorylation of the SRC-family kinase (SFK) YES and the subsequent expansion of a CD24+ cell population which showed increased metastatic behavior in vitro and in vivo relative to isogenic CD24- cells. These results suggest that LKB1 inactivation in the context of RAS activation facilitates metastasis by inducing a SFK-dependent expansion of a pro-metastatic, CD24+ tumor sub-population reference x sample

2012-06-24 | E-GEOD-34866 | biostudies-arrayexpress

LKB1/STK11 Inactivation Leads to Expansion of Pro-Metastatic Tumor Sub-Population in Melanoma

2012-06-25 | GSE34866 | GEO

AXL targeting restores PD-1 blockade sensitivity of STK11/LKB1 mutant NSCLC through expansion of TCF1+ CD8 T cells

Project description:Mutations in STK11/LKB1 in non-small cell lung cancer (NSCLC) are associated with poor patient responses to immune checkpoint blockade (ICB) and introduction of a Stk11/Lkb1 (L) mutation into murine lung adenocarcinomas driven by mutant Kras and Trp53 loss (KP) resulted in an ICB refractory syngeneic KPL tumor. Mechanistically this occurred because KPL mutant NSCLCs lacked TCF1-expressing CD8 T cells, a phenotype recapitulated in human STK11/LKB1 mutant NSCLCs. Systemic inhibition of Axl results in increased type I interferon secretion from dendritic cells that expanded tumor-associated TCF1+ PD-1+ CD8 T cells, restoring therapeutic response to PD-1 ICB for KPL tumors. This was observed in syngeneic immunocompetent mouse models and in humanized mice bearing STK11/LKB1 mutant NSCLC human tumor xenografts. NSCLC patients with identified STK11/LKB1 mutations receiving bemcentinib and pembrolizumab demonstrated objective clinical response to combination therapy. We conclude that AXL is a critical targetable driver of immune suppression in STK11/LKB1 mutant NSCLC.

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LKB1/STK11 Is a Tumor Suppressor in the Progression of Myeloproliferative Neoplasms

Project description:The myeloproliferative neoplasms (MPN) frequently progress to blast phase disease, an aggressive form of acute myeloid leukemia. To identify genes that suppress disease progression, we performed a focused CRISPR/Cas9 screen and discovered that depletion of LKB1/Stk11 led to enhanced in vitro self-renewal of murine MPN cells. Deletion of Stk11 in a mouse MPN model caused rapid lethality with enhanced fibrosis, osteosclerosis, and an accumulation of immature cells in the bone marrow, as well as enhanced engraftment of primary human MPN cells in vivo. LKB1 loss was associated with increased mitochondrial reactive oxygen species and stabilization of HIF1α, and downregulation of LKB1 and increased levels of HIF1α were observed in human blast phase MPN specimens. Of note, we observed strong concordance of pathways that were enriched in murine MPN cells with LKB1 loss with those enriched in blast phase MPN patient specimens, supporting the conclusion that STK11 is a tumor suppressor in the MPNs.

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Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and Stk11-/- Endothelial cell Transcriptomes [LKB1]

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare NGS-derived endothelial cell transcriptome profiling (RNA-seq) to microarray and quantitative reverse transcription polymerase chain reaction (qRT–PCR) methods and to evaluate protocols for optimal high-throughput data analysis

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Genome-wide analysis of Schwann cell gene expression in LKB1-SCKO mutant mice prior to occurrence of axon degeneration

Project description:Analysis of gene expression in LKB1(Stk11)-depleted sciatic nerves (LKB1-SCKO) vs control nerves from age-matched mice. Gene expression profiles are predominantly derived from Schwann cell glia and provide important information about the response of peripheral nerve Schwann cells to inactivation of the metabolic regulator protein LKB1(aka Stk11). Total RNA obtained from sciatic nerve segments from 6 LKB1-SCKO mutant mice compared to RNA from nerve segments from 6 control mice (floxed LKB1 mutant mice that do not express Cre recombinase).

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Gene expression profiling of mouse MPN cells with or without STK11 knockout

Project description:We performed RNA-sequencing of mouse cells derived from colony forming assays (CFA) to evaluate the transcriptome of MPN cells with deletion of the tumor suppressor STK11/LKB1 and relative controls. The CFA are from mouse primary floxed STK11 hematopoietic stem and progenitor cells (HSPCs) transduced with retroviruses encoding the MPN mutation MPLW515L and CRE recombinase to delete STK11.

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Genome-wide analysis of Schwann cell gene expression in LKB1-SCKO mutant mice prior to occurrence of axon degeneration

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Expression profile of A459 cells upon LKB1 expression

Project description:The purpose of the experiment is to study the expression profiles variations upon the expression of the wild type isoform of LKB1 (STK11) in human lung carcinoma A459 cells. These cells are KRAS mutated and null for STK11. Cells were previously infected with the lentiviral construct pLenti-rtTA2-IRES-H2B-GFP doxycycline-inducible plasmid (obtained from S. Tenbaum, HG Palmer’s Lab Vall d´Hebron Institute of Oncology, VHIO) containing the human STK11wild type cDNA.

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