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Long non-coding RNA Expression Profiling in Lung Cancer = Lung Adenocarcinoma (Lu-T) and in normal lung tissue (Lu-N)

ABSTRACT: The expression of long non-coding RNAs - lncRNAs - was profiled in the lung adenocarcinoma patient samples (LUAD, Lu-T) and in normal lung tissues adjacent to tumors (Lu-N) using the Invitrogen NCode Human lncRNA Array Platform. will be published in: Anna Roth et al., Restoring LINC00673 expression triggers cellular senescence in lung cancer

ORGANISM(S): Homo sapiens

PROVIDER: GSE113852 | GEO | 2019/01/23

REPOSITORIES: GEO

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Long non-coding RNA Expression Profiling in Lung Cancer = Lung Adenocarcinoma (Lu-T) and in normal lung tissue (Lu-N)

Project description:Long non-coding RNA Expression Profiling in Lung Cancer = Lung Adenocarcinoma (Lu-T) and in normal lung tissue (Lu-N)

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Comparison of gene expression in erythroblasts with the In(Lu) phenotype with normal erythroblasts.

Project description:In order to elucidate the molecular mechanism giving rise to the rare In(Lu) type of Lu(a-b-) blood group phenotype we compared the transcriptome of normal and In(Lu) erythroblasts at different stages of maturation. Many erythroid-specific genes had reduced transcript levels suggesting the phenotype resulted from a transcription factor abnormality. A search for mutations in erythroid transcription factors revealed mutations in the promoter or coding sequence of EKLF in 21 of 24 individuals with the In(Lu) phenotype. In all cases the mutant EKLF allele occurred in the presence of a normal EKLF allele. Individuals with the In(Lu) phenotype have no reported pathology indicating that one functional EKLF allele is sufficient to sustain human erythropoiesis. These data provide the first description of inactivating mutations in human EKLF and the first demonstration of a blood group phenotype resulting from mutations in a transcription factor. Keywords: Time course and cell type comparison.

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Project description:Lung cancer is the leading cause of cancer-related deaths worldwide and lung adenocarcinoma is the most common form of lung cancer. Genomic studies of lung adenocarcinoma (LUAD) have advanced our understanding of the disease's biology and accelerated targeted therapy. However, the proteomic characteristics of LUAD are still insufficiently understood. Prognosis for lung cancer patients remains poor and is strongly related to the stage of disease at the time of diagnosis. Therefore, our study focuses on metastasis formation in LUAD. We performed high-performance liquid chromatography (HPLC) and electrospray ionization tandem mass spectrometry (ESI-MS/MS) on a total of 40 FFPE samples and compared proteomic profiles of primary tumors to those of matched distant metastases. Using differential expression analysis and unsupervised clustering we identified candidate proteins playing a role in metastatic spread. Selected proteins were validated by immunoblotting. Our findings give a better understanding of tumor progression and metastasis formation in LUAD and might help to develop biomarker specific therapy.

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Integrative multi-omic analysis of the SWI/SNF complex defines a new clinical subgroup of lung adenocarcinoma patients

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Project description:Lung cancer is the most frequent cancer-related cause of death, and adenocarcinoma (LUAD) is the most frequent type. Despite the recent success of immunotherapies, survival of lung cancer patients has not significantly improved in the last decades. New therapies are necessary. We have previously identified sodium-glucose transporter 2 (SGLT2) as the major responsible for glucose uptake in LUAD, and we have showed that treatment with SGLT2 inhibitors significantly delays LUAD development and prolongs survival in murine models. However, our data shows that SGLT2 inhibitors also induce de-differentiation of LUAD cells, leading to a more aggressive phenotype and increased resistance to cisplatin. Glucose deprivation causes reduced αKG levels, leading to reduced activity of αKG-dependent histone demethylases and consequent histone hypermethylation. Supplementation of αKG or inhibition of the histone methyltransferase EZH2 reverse this phenotype, suggesting that this de-differentiated phenotype depends on insufficiency of αKG-dependent histone demethylases and unbalanced EZH2 activity. Consistently, double treatment with an SGLT2 inhibitor and an EZH2 inhibitor significantly reduces the tumor burden in a genetically engineered murine model of LUAD. We further characterized the effect of low glucose-induced tumor de-differentiation, identifying stabilization of hypoxia inducible factor 1α (HIF1α) as a major pathway responsible for the acquisition of a more aggressive phenotype following glucose deprivation. Finally, we identified an HIF1α-dependent transcriptional signature with prognostic significance in human LUAD. Our studies further our knowledge of the relationship between glucose metabolism and cell differentiation in cancer, characterizing the epigenetic adaptation of cancer cells to nutrient deprivation and identifying novel targets to prevent the development of resistance to metabolic therapies.

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Project description:The expression of long non-coding RNAs - lncRNAs - was profiled in the liver cancer Hepatocellular Carcinoma - HCC - and in normal liver tissues using the Invitrogen NCode Human lncRNA Array Platform.

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