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The Role of Lkb1 in Mouse Lung Squamous Cell Carcinoma (SCC) Development

ABSTRACT: Lung cancer, majorly divided into non-small cell lung cancer (80-85%) and small cell lung cancer (15-20%), is the leading cause of cancer death in USA. Squamous Cell Carcinoma (SCC) is one of major subtypes of non-small cell lung cancer. Although genomic analysis of tumors from SSC patients have identified frequently mutated genes in these tumors, it’s still largely unknown which genes determine SCC development. Now we found that ablation of alone Lkb1 could induce SCC around 12 months of age. Therefore, transcriptome analysis of lung SCC of CCSPiCreLkb1f/f mice will help us understand how Lkb1 regulates the development of lung SCC.

ORGANISM(S): Mus musculus

PROVIDER: GSE111313 | GEO | 2019/03/01

REPOSITORIES: GEO

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The expression profile of lung sqaumous cell carcinoma (SCC) and adenosquamous carcninoma (ASC) of CCSPiCreLkb1f/fPtenf/f mice

Project description:Lung cancer, majorly divided into non-small cell lung cancer (80-85%) and small cell lung cancer (15-20%), is the leading cause of cancer death in USA. Squamous Cell Carcinoma (SCC) is one of major subtypes of non-small cell lung cancer. Although genomic analysis of tumors from SSC patients have identified frequently mutated genes in these tumors, it’s still largely unknown which genes determine SCC development. Now we found that ablation of Lkb1 and Pten could induce SCC and ASC around 3 months of age. Therefore, transcriptome analysis of lung SCC and ASC of CCSPiCreLkb1f/f mice will help us understand how Lkb1 and Pten regulate the development of lung SCC and ASC.

2019-03-01 | GSE111335 | GEO

The Role of JNK1/2 in Mouse Lung Squamous Cell Carcinoma (SCC) Development

Project description:Lung cancer is the leading cause of cancer death in USA. Squamous Cell Carcinoma (SCC) is one of the subtypes of lung cancer. It is still largely unknown which genes or pathways regulate lung SCC development. Recently, we found JNK1/2 pathway was inhibited in mouse lung SCC induced by double ablation of Pten and Lkb1 in mouse lung epithelial cells. Now we aim to identify a genome-wide molecular signature of JNK1/2 signaling in mouse squamous cell carcinoma cells and determine pathways that transduce JNK1/2 signaling.

2019-03-01 | GSE111314 | GEO

The Role of Lkb1 in Mouse Lung Squamous Cell Carcinoma (SCC) Development

Project description:The Role of Lkb1 in Mouse Lung Squamous Cell Carcinoma (SCC) Development

| PRJNA436645 | ENA

Loss of Lkb1 and Pten Leads to Lung Squamous Cell Carcinoma with Elevated Pdl1 Expression: Stroma Cells

Project description:Lung squamous cell carcinoma (SCC) is a deadly disease for which current treatments are inadequate. We demonstrate that bi-allelic inactivation of Lkb1 and Pten in the mouse lung led to SCC that recapitulated the histology, gene expression and microenvironment found in human disease. Lkb1/Pten-null (LP) tumors expressed the squamous markers Krt5, p63 and Sox2, and transcriptionally resembled the basal subtype of human SCC. In contrast to mouse adenocarcinomas, the LP tumors contained immune populations enriched for tumor-associated neutrophils. Sca1+/Ngfr+ fractions were enriched for tumor propagating cells (TPCs) that could serially transplant the disease in orthotopic assays. TPCs in the LP model and Ngfr+ cells in human SCCs highly expressed Pdl1, suggesting a novel mechanism of immune escape for TPCs. We used microarrays to detail the gene expression profles among lung SCC tumor epitheial cell, lung ADC tumor epithelia cell and normal epithelial cells. Kras tumor stroma cells and LP tumor stroma cells were sorted by FACS, the cells were gated as EpCAM-/CD45+/CD31+

2014-01-24 | E-GEOD-54352 | biostudies-arrayexpress

Loss of Lkb1 and Pten Leads to Lung Squamous Cell Carcinoma with Elevated Pdl1 Expression: Epithelial Cells

Project description:Lung squamous cell carcinoma (SCC) is a deadly disease for which current treatments are inadequate. We demonstrate that bi-allelic inactivation of Lkb1 and Pten in the mouse lung led to SCC that recapitulated the histology, gene expression and microenvironment found in human disease. Lkb1/Pten-null (LP) tumors expressed the squamous markers Krt5, p63 and Sox2, and transcriptionally resembled the basal subtype of human SCC. In contrast to mouse adenocarcinomas, the LP tumors contained immune populations enriched for tumor-associated neutrophils. Sca1+/Ngfr+ fractions were enriched for tumor propagating cells (TPCs) that could serially transplant the disease in orthotopic assays. TPCs in the LP model and Ngfr+ cells in human SCCs highly expressed Pdl1, suggesting a novel mechanism of immune escape for TPCs. We used microarrays to detail the gene expression profles among lung SCC tumor epitheial cell, lung ADC tumor epithelia cell and normal epithelial cells. Normal EpCAM+, Kras tumor EpCAM+ and LP tumor EpCAM+ were sorted by FACS, the cells were gating as EpCAM+/CD45-/CD31-

2014-01-24 | E-GEOD-54351 | biostudies-arrayexpress

Identification of long non-coding RNAs associated with aberrant LKB1 signaling

Project description:The LKB1 tumor suppressor gene is frequently mutated and inactivated in many cancers, particularly non-small cell lung carcinoma (NSCLC). LncRNAs are a novel class of gene regulators with newly discovered roles in cancer development and progression. LncRNA involvement in altered LKB1 signaling in lung cancer is currently unknown. To investigate whether lncRNAs contribute to loss of LKB1 tumor suppression in lung tumorigenesis and maintenance, we performed genome-wide lncRNA transcriptional profiling to identify lncRNAs associated with aberrant LKB1 signaling.

2016-12-31 | GSE73414 | GEO

LKB1 modulates lung cancer differentiation and metastasis

Project description:Inherited mutation in LKB1 results in the Peutz-Jeghers syndrome (PJS), characterized by intestinal hamartomas and a modestly increased frequency of gastrointestinal and breast cancer1. Somatic inactivation of LKB1 occurs in human lung adenocarcinoma2-4, but its tumor suppressor role in this tissue is unknown. Here we show that somatic Lkb1 deficiency strongly cooperates with somatic K-rasG12D activating mutation to accelerate the development of mouse lung tumorigenesis. Lkb1 deficiency in the setting of K-rasG12D mutation (K-ras Lkb1L/L) was associated with decreased tumor latency and increased tumor aggressiveness including metastasis. Furthermore, tumors from K-ras Lkb1L/L mice demonstrated histologies--squamous, adenosquamous and large cell--not seen with K-rasG12D mutation, Ink4a/Arf inactivation, or p53 inactivation alone or in combination. Experiments in vitro suggest that LKB1 suppresses lung tumorigenesis and progression through both p16INK4a-ARF-p53 dependent and independent mechanisms. These data indicate that LKB1 regulates lung tumor progression and differentiation. Keywords: cancer research To analyze the role of LKB1 in lung cancer progression and differentiation, we have dissected the lung tumors from mice with/without lkb1 loss and performed the microarray analyses to compare their gene expression pattern. In addition, we have also performed microarray analysis in both A549 and H2126 cell lines after reconsistitution of either wt-lkb1 or the kinase dead form of lkb1 (lkb1-KD) to confirm what we observed from in vivo studies.

2007-08-28 | E-GEOD-6135 | biostudies-arrayexpress

Loss of Lkb1 and Pten Leads to Lung Squamous Cell Carcinoma with Elevated Pdl1 Expression: Stroma Cells

2014-01-24 | GSE54352 | GEO

Loss of Lkb1 and Pten Leads to Lung Squamous Cell Carcinoma with Elevated Pdl1 Expression: Epithelial Cells

2014-01-24 | GSE54351 | GEO

Lkb1 inactivation drives lung cancer lineage switching governed by Polycomb Repressive Complex 2

Project description:Adenosquamous lung tumors may result from cellular plasticity. We demonstrate lineage switching of KRAS+ lung adenocarcinomas (ADC) to squamous cell carcinoma (SCC) through deletion of Lkb1 (Stk11) in autochthonous and transplant models. Chromatin analysis reveals loss of H3K27me3 and gain of H3K27ac and H3K4me3 at squamous lineage genes, included Sox2, ΔNp63 and Ngfr. SCC lesions have higher levels of the H3K27 methyltransferase EZH2 than the ADC lesions, but there is a clear lack of the essential Polycomb Repressive Complex 2 (PRC2) subunit EED in the SCC lesions.

2017-02-02 | GSE94365 | GEO

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