We report the gene expression profiles of normal epithelial and carcinoma cell populations that differ in their relative levels of integrin-beta 4 expression. ITGB4 high, mesenchymal subtype, triple-negative breast cancer cells were found to be more epithelial than related ITGB4 low cells. Overall design: RNA-seq was used to compare the expression of mesenchymal-like carcinoma cell subtypes isolated from polyclonal cell populations. Isolated cell populations that had high levels of ITGB4 were found to be more epithelial than those with low levels, despite the fact that they were within the mesenchymal-like cell state spectrum.
Integrin-β4 identifies cancer stem cell-enriched populations of partially mesenchymal carcinoma cells.
Specimen part, Cell line, Subject
View SamplesEpigenetic mechanisms including histone post-translational modifications control longevity in diverse organisms. Relatedly, loss of proper transcriptional regulation on a global scale is an emerging aspect of shortened lifespan, but the specific mechanisms linking these observations remain to be uncovered. Here, we describe a lifespan screen in S. cerevisiae, designed to identify altered amino acid residues of histones that alter yeast replicative aging. Our results reveal that lack of sustained H3K36 methylation is commensurate with increased cryptic transcription in a set of genes in old cells and shorter lifespan. Deletion of the K36me2/3 demethylase Rph1 increases H3K36me3 within these genes and suppresses cryptic transcript initiation to extend lifespan. We show that this aging phenomenon is conserved, as cryptic transcription also increases in old worms. We propose that epigenetic misregulation in aging cells leads to an increase in transcriptional noise that is detrimental to lifespan, and, importantly, this acceleration in aging can be reversed by restoring transcriptional fidelity. Overall design: This study examines transcription in yeast aging using a WT or Rph1 mutant background over a sequence of time-dependent FACS sorts of old cells. Cryptic transcripts are detected using a small fragment sequencing approach. The youngest WT yeast (designated S1Y, S2Y) are represented in seven biological replicates and one technical replicate, five small fragment and three others; the oldest WT yeast (designated S4O) are also represented in seven biological replicates and one technical replicate, again composed of five small fragment samples and three others. Intermediate WT yeast aging sorts (S2O and S3O) are each represented by five biological replicates and one technical replicate, three small fragment and three others. For mutant yeast, each stage in the time series is represented by five biological replicates and one technical replicate, three small fragment and three others. Experiment 4 is a technical replicate of experiment 3.
H3K36 methylation promotes longevity by enhancing transcriptional fidelity.
Subject
View SamplesEpigenetic mechanisms including histone post-translational modifications control longevity in diverse organisms. Relatedly, loss of proper transcriptional regulation on a global scale is an emerging aspect of shortened lifespan, but the specific mechanisms linking these observations remain to be uncovered. Here, we describe a lifespan screen in S. cerevisiae, designed to identify altered amino acid residues of histones that alter yeast replicative aging. Our results reveal that lack of sustained H3K36 methylation is commensurate with increased cryptic transcription in a set of genes in old cells and shorter lifespan. Deletion of the K36me2/3 demethylase Rph1 increases H3K36me3 within these genes and suppresses cryptic transcript initiation to extend lifespan. We show that this aging phenomenon is conserved, as cryptic transcription also increases in old worms. We propose that epigenetic misregulation in aging cells leads to an increase in transcriptional noise that is detrimental to lifespan, and, importantly, this acceleration in aging can be reversed by restoring transcriptional fidelity. Overall design: This study examines transcription in worm aging using FUDR treatment. The samples represent a time-series, with one control group without FUDR, and then three treated with FUDR at days 1, 8, and 12. Days 8 and 12 represent old worms. There are no replicates.
H3K36 methylation promotes longevity by enhancing transcriptional fidelity.
Cell line, Treatment, Subject
View SamplessiRNAs with dN are a promising and easy approach to characterize essential genes by minimizing the off-target effect in cancer cells. Overall design: mRNA profiles of HCT 116 cells after the transfection of siRNAs or blank control by deep sequencing, using HiSeq 2000
siRNAs with decreased off-target effect facilitate the identification of essential genes in cancer cells.
No sample metadata fields
View SamplesTo identify genes affected by mutant huntington protein, we performed mRNA-seq experiments with Striatal STHdh Q7/Q7, Q7Q111, and Q111/Q111 cells. We also tested the effect of Sp1 overexpression on rescuing gene expression in Q111/Q111 cells. Overall design: Striatal STHdh Q7/Q7, Q7/Q111 and Q111/Q111 cells were used for the mRNA-seq in replicates. After Sp1 transient overexpression in Q111/Q111 cells, cells were collected for mRNA-seq analysis.
Real-time imaging of Huntingtin aggregates diverting target search and gene transcription.
Specimen part, Cell line, Subject
View SamplesWe compared molecular characteristics of primary and recurrent pediatric ependymoma to identify sub-group specific differences.
Molecular sub-group-specific immunophenotypic changes are associated with outcome in recurrent posterior fossa ependymoma.
Specimen part
View SamplesWe reported the transcriptional profiles of E.coli expressing antimicrobial peptide LL37 under stress response condition. Overall design: 4 samples, two groups, one group is under aerobic condition, the other group is under anaerobic condition. One of samples is E.coli which expressed LL37 as induction in each group, another sample is E.coli with no LL37 expression in vivo as control in each group.
Effect of intracellular expression of antimicrobial peptide LL-37 on growth of escherichia coli strain TOP10 under aerobic and anaerobic conditions.
Cell line, Subject
View SamplesTreatment of triple-negative breast cancer has been challenging and paclitaxel resistance is one of the major obstacles to the better prognosis. Misregulation of alternative splicing (AS) may contribute to tumor progression and chemotherapy resistance. Human AS factor TRA2 has two separate gene paralogs encoding TRA2A and TRA2B proteins. TRA2B is associated with cancer cell survival and therapeutic sensitivity.
TRA2A Promoted Paclitaxel Resistance and Tumor Progression in Triple-Negative Breast Cancers via Regulating Alternative Splicing.
Cell line
View SamplesIn this study we investigated the gene expression profiling in three HCC cell lines with different organ-tropism.The parent cell line has low metastasis ability in nude mice model. Subclone 1 has higher metastasis ability specific to lung, and subclone 2 has dual metastasis ability to lung and celiac lymph node. We aimed to explore differentially expressed genes involved in process of HCC metastasis and organ-specific metastasis, and identify their biological functions. Overall design: Examination of different gene expression among the 3 cell types.
Establishment of monoclonal HCC cell lines with organ site-specific tropisms.
Specimen part, Cell line, Subject
View SamplesAlterations of TWIST-1 expression are often seen in solid tumors and contribute to tumorigenesis and cancer progression. However, studies concerning its pathogenic role in leukemia are scarce. Here we show that TWIST-1 is a new candidate gene contributing to leukemogenesis of myeloid leukemia.
TWIST-1 promotes cell growth, drug resistance and progenitor clonogenic capacities in myeloid leukemia and is a novel poor prognostic factor in acute myeloid leukemia.
Specimen part, Cell line
View Samples