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Nanog maintains the stemness of Lkb1-deficient lung adenocarcinoma and prevents gastric differentiation

ABSTRACT: We here find that Lkb1-deficient lung tumors from KL model harbor stronger stemness and show the upregulation of Nanog expression in contrast to KrasG12D/+ or KrasG12D/+; P53-/- tumors.

TISSUE(S): Lung

DISEASE(S): Lung Adenocarcinoma

SUBMITTER: Xinyuan,Tong

PROVIDER: OEX002292 | NODE |

REPOSITORIES: NODE

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ECM-enriched mouse lung - TMT-based quantitative mass spectrometry analysis was performed on ECM-enriched preparation from normal murine lung, bleomycin-induced fibrotic lung, primary tumors and lymph node metastasis isolated from the KrasG12D/+p53-/- mouse model of lung adenocarcinoma. Three independent samples were processed and analyzed for each condition. This study identified ECM signatures of normal and diseased lung tissue.

Project description:TMT-based quantitative mass spectrometry analysis was performed on ECM-enriched preparation from normal murine lung, bleomycin-induced fibrotic lung, primary tumors and lymph node metastasis isolated from the KrasG12D/+p53-/- mouse model of lung adenocarcinoma. Three independent samples were processed and analyzed for each condition. This study identified ECM signatures of normal and diseased lung tissue.

2017-06-21 | PXD003517 | Pride

Bulk-ATAC sequencing in RUNX-altered murine lung adenocarcinoma cell lines

Project description:Here, we using CRISPR activation and knockout studies to assess the implication of dysregulation of RUNX transcription factors on chromatin accessibility using bulk ATAC-sequencing. Tumor cell lines were derived from primary Kras G12D; p53 mutant mice (KP model) after initiation of tumors with SPC-Cre, resulting in lung adenocarcinoma. Cell lines were then expanded and profiled using bulk ATAC-sequencing.

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Lung adenocarcinoma invasion and progression

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2011-09-14 | E-GEOD-27719 | biostudies-arrayexpress

Single-cell epigenomics identifies a premetastatic regulatory program in lung adenocarcinoma [sciATAC-seq]

Project description:Here we use an improved single-cell chromatin profiling approach to determine epigenomic alterations across tumor progression in a mouse model of lung adenocarcinoma (LUAD). Specifically, we induced tumors by providing Adeno-SPC-Cre virus to mice intratracheally to induce tumors due to conditional expression the Kras G12D mutation and loss of p53 (termed the KPT model). Mice also expressed a tdTomato reporter allele allowing for the sorting of tumor cells in late-stages of tumor progression. Using a combinatorial indexing approach (sciATAC-seq), we identify an epigenomic continuum representing a loss of cellular identity and progression towards a metastatic state.

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Single-cell epigenomics identifies a premetastatic regulatory program in lung adenocarcinoma [scATAC-seq]

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Mouse small cell lung cancer model

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Identification of Metastasis-prone Lung Adenocarcinoma Cell Population That Is Sensitive to Notch Inhibition

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The lung-enriched p53 mutants V157F and R158L/P regulate a novel transcriptome in lung cancer

Project description:Lung cancer is the leading cause of cancer-related deaths in the US, and alterations in the tumor suppressor gene TP53 are the most frequent somatic mutation among all histologic subtypes of lung cancer. Mutations in TP53 frequently result in a protein that exhibits not only loss of tumor suppressor capability but also gain of oncogenic function (GOF). The canonical p53 hotspot mutants R175H and R273H, for example, confer upon tumors a metastatic phenotype in murine models of mutant p53. To our knowledge, GOF phenotypes of the less often studied V157, R158, and A159 mutants – which occur with higher frequency in lung cancer compared with other solid tumors – have not been defined. In this study, we aimed to define whether the lung mutants are simply equivalent to full loss of the p53 locus, or whether they additionally acquire the ability to drive new downstream effector pathways. Using a publicly available human lung cancer dataset, we characterized patients with V157, R158, and A159 p53 mutations. Additionally, we show here that cell lines with mutant p53-V157F, p53-R158L, and p53-R158P exhibit a loss of expression of canonical wildtype p53 target genes. Furthermore, these lung-enriched p53 mutants regulate genes not previously linked to p53 function including PLAU. Paradoxically, mutant p53 represses genes associated with increased cell viability, migration, and invasion. These findings collectively represent the first demonstration that lung-enriched p53 mutations at V157 and R158 regulate a novel transcriptome in human lung cancer cells and may confer de novo function.

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2024-05-08 | GSE266561 | GEO

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