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Whole transcriptome (gene expression and splice isoform changes) profiling using Affymetrix Human Transcriptome Array 2.0

ABSTRACT: Transcriptome analysis of total RNA samples from human cell line (LAM 621-101, female) Global gene and splice isoform expression profiling was performed to get a comprehensive view of transcriptome changes in human Lymphangioleiomyomatosis (LAM 621-101, female) cell line after inhibition of mTORC1 and SRPK2 proteins.

ORGANISM(S): Homo sapiens

PROVIDER: GSE104335 | GEO | 2017/09/28

SECONDARY ACCESSION(S): PRJNA412383

REPOSITORIES: GEO

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Expression data from LAM-associated fibroblasts and normal human lung fibroblasts co-cultured with TSC2-/- 621-101 cells

Project description:Patients with Lymphangioleiomyomatosis (LAM) develop nodules of cells within the lung parenchyma. These lesions contain both TSC2-/- LAM cells, and wild type fibroblasts. We investigated the effect of TSC2-/- cells on the transcriptional profile of both normal fibroblasts and fibroblasts isolated from LAM patient tissue (LAFs) using Affymetrix Gene Chip arrays, to identify upregulated pathways which could contribute to LAM pathology. We used Affymetrix microarrays to detail the changes in the global profile of gene expression in fibroblasts following co-culture with 621-101 cells, and identified upregulation of several chemokines, indicating that the fibroblasts had adopted an inflammatory phenotype.

2021-12-31 | GSE160618 | GEO

RNA-seq analysis the whole transcriptome in MCF7 cells

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Transcriptomic Differences Associated with TSC2 Gene Expression Loss in Lymphangioleiomyomatosis [human cells]

Project description:Pulmonary Lymphangioleiomyomatosis (LAM), a rare lung disease that affects predominantly women, is characterized by proliferation of smooth muscle-like cells in the lungs, destruction of lung tissue, upregulation of VEGF-D, and growth of lymphatic vessels inducing a loss of pulmonary function. TSC2 gene mutations that render TSC2 inactive are a common finding associated with LAM. To better understand the function of the TSC2 gene in LAM , we sought to characterize differences in the transcriptome of cells where TSC2 is inactivated. RNA-Seq was used to measure transcript expression differences between a human TSC2-null angiolipoma cell line derived from an individual with LAM, and the same cell line with re-expressed TSC2 to serve as a control. The Illumina TruSeq method was used to prepare poly(A)-selected stranded RNA-Seq libraries, and 100bp paired-end reads were generated with an Illumina Hi-Seq 2500 instrument in high output mode. RNA-Seq data was analyzed using kallisto (http://pachterlab.github.io/kallisto/) and R.

2018-05-23 | GSE84476 | GEO

Therapeutic benefit of rapamycin combined with clorgyline or rasagiline in an immunodeficient LAM model

Project description:Inhibition of mechanistic target of rapamycin (mTOR) constitutes the standard of care of lymphangioleiomyomatosis (LAM). However, this treatment does not eradicate diseased cells and some patients show progressive decline of lung function. This study provides preclinical evidence for beneficial therapeutic approaches in combination with rapamycin. LAM tumorigenesis is reduced in vivo (ELT3-V3 tumor xenografts) using approved drugs for other human diseases and targeting monoamine oxidase A (MAO-A; clorgyline) or MAO-B (rasagiline).

2019-10-01 | GSE129399 | GEO

Transcript profiling of Lymphangioleiomyomatosis (LAM) nodules in Human Patients

Project description:Lymphangioleiomyomatosis (LAM) is characterized by cystic lung destruction caused by smooth, muscle-like LAM cells which have mutations in the tumor suppressor genes Tuberous Sclerosis Complex (TSC) 1 or 2, and the capacity to metastasize. Since chemokines and their receptors function in chemotaxis of metastatic cells, we hypothesized that LAM cells may be recruited by chemokine(s) in the lung. Quantification of 25 chemokines in bronchoalveolar lavage fluid from LAM patients and healthy volunteers revealed that concentrations of MCP-1/CCL2, GROa/CXCL1 and ENA-78/CXCL5 were significantly higher in samples from LAM patients than healthy volunteers. In this transcript analysis, expression of chemokine and chemokine receptor mRNA in LAM cells differed from those in melanoma and smooth muscle cells. Subsequent immunohistochemistry of lung sections from 30 LAM patients confirmed protein expression of chemokines and these receptors varied among LAM patient and differed from that seen in breast cancer and melanoma cells. . In vitro, MCP-1/CCL2 induced selective migration of cells showing loss of heterozygosity of TSC2 from a heterogeneous populations of cells grown from explanted LAM lungs. In addition, the frequencies of single-nucleotide polymorphisms in the MCP-1 gene promoter region differed significantly in LAM patients and healthy volunteers (p=0.018), and one polymorphism was associated significantly more frequently with the decline of lung function. These observations are consistent with the notion that chemokines such as MCP-1 may serve to specify site of LAM cell metastasis. Keywords: Human patient sample comparison with cell lines The study is of case/control design with biological replication. Biopsies of nodules from 14 LAM patients (cases) are compared with cultured cell lines (controls) with similar properties.

2008-12-30 | E-GEOD-12027 | biostudies-arrayexpress

Gene expression profiling of 621-101 cells with rapamycin treatment and Rheb downregulation

Project description:621-101 cells were treated with rapamycin and rhebsiRna and samples were run in triplicates for each condition.

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Project description:Lymphangioleiomyomatosis (LAM) is a rare, debilitating lung disease that predominantly affects women of reproductive age. LAM cells carry deleterious mutations of tuberous sclerosis complex (TSC1/TSC2) genes, resulting in hyperactivation of the mechanistic target of rapamycin complex 1 (mTORC1) and ultimately dysregulated cell growth. The integrative single cell omics data identified the activation of uterine specific HOX-PBX transcriptional programming in pulmonary LAMCORE cells. Network analysis predicted homeobox transcription factors including PBX1 and HOXD11 as key regulators controlling LAMCORE cell fate. Targeting the HOX-PBX network may have therapeutic value in LAM and TSC-related diseases, and possibly in other mTORC1-hyperactive neoplasms.

2023-04-03 | GSE217107 | GEO

Integrative Single Cell Multiomic Profiling Analysis Reveals HOX-PBX Gene Regulatory Network Regulating the Survival of mTOR Hyperactive Cells [snATAC-Seq]

2023-04-03 | GSE217106 | GEO

Multicenter International Lymphangioleiomyomatosis Efficacy of Sirolimus Trial (The MILES Trial)

Project description:<p>Lymphangioleiomyomatosis (LAM) is an uncommon, progressive, cystic lung disease that predominantly affects young women. It is believed to be caused by defects within cellular pathways that regulate nutrient uptake, cell size, cell migration, and cell proliferation. The disease is caused by mutations in tuberous sclerosis complex (TSC) genes. Individuals with Lymphangioleiomyomatosis (LAM) often experience pneumothorax and chylothorax, as well progressive loss of lung function. Lymphangioleiomyomatosis (LAM) is frequently fatal and existing therapies for the disease have not proven effective. Lung transplantation can be considered as a last option, but alternative treatments are needed. Sirolimus is an immunosuppressive drug that is often used in people who have had kidney transplants. It directly affects the genetic pathway that causes Lymphangioleiomyomatosis (LAM). This study will evaluate the safety and effectiveness of sirolimus in stabilizing or improving lung function in people with Lymphangioleiomyomatosis (LAM).</p> <p>Individuals interested in participating in this 2-year, double-blind study will first report to the study sites for pulmonary function testing to determine their eligibility for participation. Participants deemed eligible will be randomly assigned to receive either sirolimus or placebo for 1 year. Sirolimus or placebo will be administered in 2 tablet doses (2 mg for sirolimus) for the duration of the study. Study visits will occur at baseline, Week 3, every 3 months for 12 months, and Months 18 and 24. Study visits will include a physical exam, questionnaires, a pregnancy test, blood and urine collection, and functional lung tests. A 6-minute walk test will occur at most study visits; a chest x-ray will be taken at baseline and Month 24; and a volumetric computed tomography scan will occur at baseline Month 12, and Month 24. Adverse events, medication side effects, and lung function will be assessed at each visit.</p>

| phs000605 | dbGaP

Investigation of the gene expression changes triggered by the lung mesenchymal Tsc2KO in each major cell subpopulation of the adult mouse lung

Project description:Tumor suppressor Tuberous sclerosis complex 2 (TSC2) is a key negative regulator of mammalian target of rapamycin (mTOR), a central controller of cell growth and metabolism in health and disease. Loss of TSC2 induces the constitutive activation of mTORC1 in rare lung disease pulmonary Lymphangioleiomyomatosis (LAM), which affects only women of childbearing age and characterized by lung destruction and progressive loss of pulmonary function. Little is known how TSC2 loss induces LAM and what is the LAM cell of origin. To determine cell-type specific effects of TSC2 loss and mTORC1 activation on lung homeostasis we generated new transgenic mice with targeted Tsc2 deletion in lung mesenchyme Tbx4-Cre+Tsc2flox/flox and lung epithelium Shh-Cre+Tsc2flox/flox. Both Tbx4-Cre+, Tsc2flox/flox and Shh-Cre+, Tsc2flox/flox mice were viable and fertile. Adult Tbx4-Cre+Tsc2flox/flox mice demonstrated mTORC1 activation in lung mesenchyme, progressive alveolar enlargement, female-specific pulmonary function decline and prgenancy-induced lesion growth. To investigate molecular mechanism underlying observed phenotypic changes in the Tsc2KO lungs we performed comparative bulk-RNAseq analysis of the gene expression changes in the major cell subpopulations of the adult female 8-week-old Tsc2KO mouse lungs compared to the age- and sex-matched WT controls.

2020-08-31 | GSE139818 | GEO

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