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Gene expression alteration by different cell lines derived from lung SCC of IKKα mutant mice

ABSTRACT: In this study, we found that kinase-dead IKKα knockin (KAL) mice. develop spontaneous lung squamous cell carcinomas (SCCs) associated with IKKα downregulation and marked pulmonary inflammation.KKα downregulation dysregulates the expression of multiple oncogenes and tumor suppressors in K5+ lung epithelial cells. The mutant macrophages increase inflammatory responses and oxidative stress to promote DNA damage in IKKα-mutant K5+ lung epithelial cells, which further dysregulate the levels of multiple oncogenes, tumor suppressors, and stem cell genes, thereby promoting the IKKαlowK5+p63hi cell transition to tumor cells in L-IkkαKA/KA lungs. To further investigate the underlying mechanisms by which the lung SCC development, we generated two cell lines, named as S1 and S2 individually, which were derived from KAL lung SCC. The S1 cells express high level of Sca1 and exhibit tumorigenic phenotype, while the S2 cells express low level of Sca1 and exhibit less tumorigenic phenotype. The aim of this microarray assay is to identify differentially expressed genes between S1 and S2 cells, which may highlight the important genes or pathways involved in inflammation-associated lung SCC carcinogenesis.

ORGANISM(S): Mus musculus

PROVIDER: GSE65291 | GEO | 2015/01/27

SECONDARY ACCESSION(S): PRJNA273638

REPOSITORIES: GEO

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Gene expression alteration by different cell lines derived from lung SCC of IKKM-NM-1 mutant mice

Project description:In this study, we found that kinase-dead IKKM-NM-1 knockin (KAL) mice. develop spontaneous lung squamous cell carcinomas (SCCs) associated with IKKM-NM-1 downregulation and marked pulmonary inflammation.KKM-NM-1 downregulation dysregulates the expression of multiple oncogenes and tumor suppressors in K5+ lung epithelial cells. The mutant macrophages increase inflammatory responses and oxidative stress to promote DNA damage in IKKM-NM-1-mutant K5+ lung epithelial cells, which further dysregulate the levels of multiple oncogenes, tumor suppressors, and stem cell genes, thereby promoting the IKKM-NM-1lowK5+p63hi cell transition to tumor cells in L-IkkM-NM-1KA/KA lungs. To further investigate the underlying mechanisms by which the lung SCC development, we generated two cell lines, named as S1 and S2 individually, which were derived from KAL lung SCC. The S1 cells express high level of Sca1 and exhibit tumorigenic phenotype, while the S2 cells express low level of Sca1 and exhibit less tumorigenic phenotype. The aim of this microarray assay is to identify differentially expressed genes between S1 and S2 cells, which may highlight the important genes or pathways involved in inflammation-associated lung SCC carcinogenesis. There were two cell lines were used to perform Gene chip assay with Affymetrix. The two cell lines, named as S1 and S2 individually, were derived from KAL lung SCC. The S1 cells express high level of Sca1 and exhibit tumorigenic phenotype, while the S2 cells express low level of Sca1 and exhibit less tumorigenic phenotype.

2015-01-27 | E-GEOD-65291 | biostudies-arrayexpress

Gene expression alteration by macrophage depletion in IKKα mutant mice

Project description:We generated Ikkα-KA/KA knock-in mice (KA/KA), in which an ATP binding site of Ikkα Lys 44 was replaced by alanine. The knock-in mice develop severe skin lesions and begin to die after 6 to 10 months. We also found lung SCCs in some of the mice. To study lung SCC development, we stabilize the skin condition by crossing KA/KA with Lori.Ikkα transgenic mice to generate KA/KA-Lori.Ikkα mice, which 100% spontaneously developed lethal lung SCC at 4 to 6 months of age. Clodronate-liposomes obtained from Dr. N. van Rooijen (Vrije Universiteit, Amsterdam, Netherlands) were intravenously injected into mice twice every week, started in 4 weeks old mice, and continued for 3 months. The dose of clodronate-liposomes was 100µl during the first month and elevated to 150 100µl after that. The depletion efficacy was confirmed by detecting pulmonary macrophages with Flow Cytometry. Depletion of macrophages in these KA/KA-Lori.Ikkα mice could significantly reduce inflammation and prevent lung SCC developmrnt. This aim of this microarray assay is to identify differentially expressed genes among Wild type, KA/KA-Lori.Ikkα, and macophage-depleted KA/KA-Lori.Ikkα mice, which may highlight the important genes or parthways involved in inflammation-associated lung SCC carcinogenesis. Three samples were analyzed: 1. WT (lung tissue from wild type mouse); 2. KA2 (mixture tissue of lung SCC and tumor neighbor from KA/KA-Lori-Ikkα mouse ); 3. KAT (lung tissue from KA/KA-Lori-Ikkα mouse with macrophage depletion treatment)

2012-04-30 | E-GEOD-37655 | biostudies-arrayexpress

Gene expression alteration by macrophage depletion in IKKα mutant mice

2012-05-01 | GSE37655 | GEO

ArrayCGH mapping of chromosome 3 aberrations in lung Squamous Cell Carcinoma (SCC)

Project description:To prospectively identify new oncogenes implicated in lung Squamous Cell Carcinoma pathogenesis, we investigated chromosome 3 aberrations in advanced tumours using arrayCGH. These aberrations are indeed among the most frequent aberrations in lung SCC and correlate with SCC patient's poor prognosis. We precisely map regions of recurrent losses at 3p and gains at 3q25-qter in a series of lung SCC. We moreover uncover 3q26.3-q27 high level amplifications in 20% of tumours. Keywords: ArrayCGH, Lung Squamous Cell Carcinoma, 3q26.3, SOX2 Profiling of 26 advanced (stage III) lung SCC. Replicates : each tumor sample is hybridized together with a normal dna sample to one microarray. Each microarray contain 3 replicates per BAC clone.

2010-05-14 | E-GEOD-14859 | biostudies-arrayexpress

ArrayCGH mapping of chromosome 3 aberrations in lung Squamous Cell Carcinoma (SCC)

2010-02-10 | GSE14859 | GEO

Expression profile analysis of circular RNAs during embryonic lung development of C57BL/6 mice

Project description:Objectives: The contribution of circular RNAs (circRNAs) in the regulation of embryonic lung development is not yet clear. This study aims to uncover the differentially expressed circRNAs in mouse embryonic lung tissue. Methods: High-throughput sequencing (HTS) was used to determine the cirRNA expression profiles at four time points of mouse embryonic lung tissue [embryonic (E) Day 14.5 (E14.5/S1), (E16.5/S2), (E18.5/S3), and newborn (N) Day 7.5 (N7.5/S4)]. CircRNAs that were significantly differential were subjected to bioinformatic analysis and functional prediction for their host genes. Finally, quantitative real-time reverse transcriptase polymerase chain reaction (qRT-PCR) was conducted to examine their levels. Results: Dynamically expressed circRNAs in the mouse embryonic lung tissue were identified. After that, a total of 231 circRNAs differentially expressed between the three groups (S1 vs. S2, S1 vs. S3 and S1 vs. S4) in embryonic lung tissue (fold change ≥ 2.0; p < 0.05). These circRNAs were subjected to bioinformatic analysis to predict their potential biological functions. Finally, six circRNAs (circRNA3_Ttn, circRNA56_Galnt18, circRNA38_Alg12, circRNA42_Filip1l, circRNA43_Ptprm, and circRNA57_Ncoa3) that were further validated using qRT-PCR. Conclusions: These findings illustrate the vital functions of circRNAs in mouse embryonic lung development. Combined with our results and previous researches, circRNAs may serve as potential miRNA sponges in the embryonic lung development. Our research is conducive to further explore the development of embryonic lungs, and the dynamic expressed circRNAs may be novel molecules that regulate mouse lung development.

2019-08-07 | GSE131839 | GEO

ArrayCGH mapping of the recurrent 3q26.3-q27 amplifications in lung Squamous Cell Carcinoma (SCC)

Project description:To prospectively identify new oncogenes implicated in lung Squamous Cell Carcinoma pathogenesis, we investigated chromosome 3 aberrations in advanced tumours using arrayCGH. Chromosome 3 aberrations are indeed among the most frequent alterations in lung SCC and correlate with SCC patient's poor prognosis. We have precisely mapped regions of recurrent losses at 3p and gains at 3q25-qter in a series of lung SCC (GSE14859) amd moreover uncover 3q26.3-q27 high level amplifications in 20% of tumours. These amplicons were precisely mapped in these tumors using arraCGH with a 3q26.3 dedicated tiling array. Keywords : ArrayCGH, lung Squamous Cell Carcinoma, 3q26.3, SOX2 Keywords: ArrayCGH Profiling of 5 advanced (stage III) lung SCC using a chromosome 3 array providing 3q26.3-q27 tiling coverage. Replicates : each array contains three replicates per clone and each sample is hybridized to two arrays, results are subsequently averaged.

2010-02-09 | E-GEOD-15079 | biostudies-arrayexpress

ArrayCGH mapping of the recurrent 3q26.3-q27 amplifications in lung Squamous Cell Carcinoma (SCC)

Project description:To prospectively identify new oncogenes implicated in lung Squamous Cell Carcinoma pathogenesis, we investigated chromosome 3 aberrations in advanced tumours using arrayCGH. Chromosome 3 aberrations are indeed among the most frequent alterations in lung SCC and correlate with SCC patient's poor prognosis. We have precisely mapped regions of recurrent losses at 3p and gains at 3q25-qter in a series of lung SCC (GSE14859) amd moreover uncover 3q26.3-q27 high level amplifications in 20% of tumours. These amplicons were precisely mapped in these tumors using arraCGH with a 3q26.3 dedicated tiling array. Keywords : ArrayCGH, lung Squamous Cell Carcinoma, 3q26.3, SOX2 Keywords: ArrayCGH

2010-02-10 | GSE15079 | GEO

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.

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

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