Project description:Lung cancer is the single most frequent cause of cancer death worldwide and is relatively more common in males. For reasons that are currently unknown, lung cancer is also associated with significantly worse outcomes in men than women. Here we examine the pulmonary transcriptome in lung cancer at a systems level through network analysis. We compare gene expression networks in affected and unaffected tissue derived from 126 patients with lung cancer. Examination of tissue-specific co-expression patterns reveals markedly poor preservation of a sex-associated gene co-expression network in tumor tissue.

2021-06-15 | GSE151101 | GEO

Evidence of Y Chromosome LncRNAs involved in Radiation Response of Male Non-Small Cell Lung Cancer Cells

Project description:Numerous studies have implicated changes in the Y chromosome in male cancers, however few have investigated the biological importance of Y chromosome non-coding RNAs. Here, we demonstrate a group of Y chromosome-expressed long non-coding RNAs (lncRNAs) involved in male non-small cell lung cancer (NSCLC) radiation sensitivity. Radiosensitive male NSCLC cell lines demonstrated a dose-dependent induction of linc-SPRY3-2/3/4 following irradiation, not observed in radioresistant male NSCLC cell lines. Cytogenetics revealed the loss of chromosome Y (LOY) in the radioresistant male NSCLC cell lines. Gain- and loss-of-function experiments indicated that linc-SPRY3-2/3/4 transcripts affect cell viability and apoptosis. UV Cross-linking and Immunoprecipitation (CLIP) and RNA stability assays identify IGF2BP3 as a binding partner for the linc-SPRY3-2/3/4 RNAs which alters the half-life of the anti-apoptotic HMGA2 mRNA as well as the oncogenic c-MYC mRNA. To assess the clinical relevance of these findings, we examined the presence of the Y chromosome in NSCLC tissue microarrays and the expression of linc-SPRY3-2/3/4 in NSCLC RNAseq and microarray data. We observed a negative correlation between the loss of the Y chromosome or linc-SPRY3-2/3/4 and overall survival. Thus, linc-SPRY3-2/3/4 expression and LOY could represent an important marker of radiation therapy in NSCLC.

2020-03-30 | GSE147708 | GEO

Activation of proto-oncogenes by disruption of chromosome neighborhoods

Project description:Activation of proto-oncogenes by disruption of chromosome neighborhoods

| PRJNA284247 | ENA

Disruption of Y chromosome expression in male lung cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-06-15 | GSE151103 | GEO

Evidence of Y Chromosome LncRNAs involved in Radiation Response of Male Non-Small Cell Lung Cancer Cells

Project description:Evidence of Y Chromosome LncRNAs involved in Radiation Response of Male Non-Small Cell Lung Cancer Cells

| PRJNA616156 | ENA

Circadian disruption enhances HSF1 signaling and tumorigenesis in Kras-driven lung cancer

Project description:Disrupted circadian rhythmicity is a prominent feature of modern society and has been designated as a probable carcinogen by the World Health Organization. However, the biological mechanisms that connect circadian disruption and cancer risk remain largely undefined. We demonstrate that exposure to chronic circadian disruption (chronic jetlag, CJL) increases tumor formation in a mouse model of KRAS-driven lung cancer. Molecular characterization of tumors and tumor-bearing lung tissues revealed that CJL enhances the expression of heat shock factor 1 (HSF1) target genes. Consistently, exposure to CJL disrupted the highly rhythmic nuclear trafficking of HSF1 in the lung, resulting in an enhanced accumulation of HSF1 in the nucleus. HSF1 has been shown to promote tumorigenesis in other systems, and we find that pharmacological inhibition of HSF1 reduces the growth of KRAS-mutant human lung cancer cells. These findings implicate HSF1 as a molecular link between circadian disruption and enhanced tumorigenesis.

2022-02-01 | GSE194097 | GEO

Activation of proto-oncogenes by disruption of chromosome neighborhoods [chIA-PET]

Project description:Mutations such as gene fusion, translocation and focal amplification are a frequent cause of proto-oncogene activation during tumorigenesis, but such mutations do not explain all cases of proto-oncogene activation. Here we show that disruption of local chromosome conformation can also activate proto-oncogenes in human cells. We mapped chromosome structures in T-cell acute lymphoblastic leukemia (T-ALL), and found that active oncogenes and silent proto-oncogenes generally occur within insulated neighborhoods formed by the looping of two interacting CTCF sites co-occupied by cohesin. Recurrent microdeletions frequently overlap neighborhood boundary sites in T-ALL genomes, and we demonstrate that site-specific perturbation of loop boundaries is sufficient to activate the respective proto-oncogenes in non-malignant cells. We found somatic genomic rearrangements affecting loop boundaries in many cancers. These results suggest that chromosome structural organization is fundamental to identify functional somatic alterations in cancer genomes.

2015-05-28 | GSE68977 | GEO

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