Osteosarcoma (OS) is the malignant bone tumor with a high tendency to metastasize to the lung, where the molecular mechanisms are unclear. The mouse OS cell line LM8 has been isolated originally from the Dunn OS cell line by in vivo selection as a subline with a high metastatic potential to the lung.
Stable knockdown of S100A4 suppresses cell migration and metastasis of osteosarcoma.
Cell line
View SamplesThe discovery of activity-dependent neuroprotective protein (ADNP) regulated tooth eruption in mice and man, provides, for the first time, an early detection of tooth eruption, with full or almost full mouth of teeth at one year of age, as a potential biomarker for an intellectual disability (ID)/autism spectrum disorder (ASD) syndrome, toward improved translational medicine. Overall design: RNAseq of 4 samples, comparing three ADNP-mutated lymphoblastoid cell lines (LCLs, derived from ADNP-mutated children) with a non-mutated cell line. No replicates were performed but results were verified usign RT-PCR.
Tauopathy in the young autistic brain: novel biomarker and therapeutic target.
Specimen part, Cell line, Subject
View SamplesNormal and diseased human tissues were profiled for gene expression using the Affymetrix U133 plus 2.0 array
Human endometriosis is associated with plasma cells and overexpression of B lymphocyte stimulator.
No sample metadata fields
View SamplesPrions consist of aggregates of abnormal conformers of cellular prion protein (PrPC). They propagate by recruiting host-encoded PrPC although the critical interacting proteins and the reasons for the differences in susceptibility of distinct cell lines and populations are unknown. We derived a lineage of cell lines with markedly differing susceptibilities, unexplained by PrPC expression differences, to identify such factors. We examined the transcriptomes of prion-resistant revertants, isolated from highly susceptible cells, and identified a gene expression signature associated with susceptibility. Several of these genes encode proteins with a role in extracellular matrix (ECM) remodelling, a compartment in which disease-related PrP deposits. Loss-of-function of nine of these genes significantly increased susceptibility. Remarkably, inhibition of fibronectin 1 binding to integrin 8 by RGD peptide inhibited metalloproteinases (MMP)-2/9 whilst increasing prion propagation rates. This indicates that prion replication may be controlled by MMPs at the ECM in an integrin-dependent manner.
Identification of a gene regulatory network associated with prion replication.
Treatment
View SamplesDrosophila miRNAs show distinct change in isoform distribution pattern with age. Some miRNAs show accumulation of the short isoforms, while other miRNAs show the accumulation of the long isoforms with age. The increase of the long isoforms of some miRNAs reflects increased 2''-O-methylated miRNA isoforms with age. The increase in 2''-O-methylated miRNA isoforms reflected increased Ago2-loading, but not Ago1-loading of specific miRNA isoforms with age. This raised a question on whether there is global shift in small RNA loading pattern between Ago1 and Ago2 with age. To investigate change in small RNA loading pattern between Ago1 and Ago2 with age, we performed small RNA deep-sequencing of Ago1 vs Ago2-IP small RNAs at 3d and 30d in Drosophila. This analysis revealed global increase of miRNA loading into Ago2, but not into Ago1 with age. Overall design: 3d and 30d FLAG-HA-Ago2 male flies were collected. Ago1 and Ago2 were immunoprecipitated by anti-Ago1 and anti-FLAG M2 beads respectively. RNA was purified from the beads, P32-labeled, and small RNA fraction was gel-purififed. Small RNA libraries were prepared using Illumina''s TruSeq small RNA sample preparation kit (#RS-200-0012, Illumina, Inc. San Diego, CA), following the manufacturer''s protocol. The libraries were multiplexed and sequenced on HiSeq2000 platform (Illumina).
Impact of age-associated increase in 2'-O-methylation of miRNAs on aging and neurodegeneration in Drosophila.
Sex, Specimen part, Subject
View SamplesA key function of Na+/H+ exchanger regulatory factor 2 (NHERF2) is spatial organization of signaling proteins to facilitate signal transduction. The role of NHERF2 in cancer progress is not well understood. This study determines how loss of NHERF2 alter colon cancer progress. Overall design: We show that loss of NHERF2 decreases colon cancer cell proliferation. To compare the effects of NHERF2 and LPA2 at the molecular level, HCT116 colon cancer xenograft with knockdown of NHERF2 or LPA2 was analyzed by RNAseq. Please note that standard cufflinks/cuffdiff output files are provided in the compressed tar files as processed data and Cufflinks/Cuffdiff output file content/formats are described at: https://cole-trapnell-lab.github.io/cufflinks/cuffdiff/#cuffdiff-output-files https://cole-trapnell-lab.github.io/cufflinks/file_formats/ (also included in the ''readme.txt'' file)
Deletion of Na+/H+ exchanger regulatory factor 2 represses colon cancer progress by suppression of Stat3 and CD24.
No sample metadata fields
View SamplesThis series contain mouse and rat lung samples treated with mechanical ventilation and corresponded controls.
Bioinformatic identification of novel early stress response genes in rodent models of lung injury.
No sample metadata fields
View SamplesMiRNAs are essential mediators of many biological processes. The aim of this study was to investigate the dynamics of miRNA-mRNA regulatory networks during exercise and subsequent recovery period.
Dynamically regulated miRNA-mRNA networks revealed by exercise.
Sex, Age
View SamplesIn some organs, adult stem cells are uniquely poised to serve as cancer cells of origin1-4. It is unclear, however, whether tumorigenesis is influenced by the activation state of the adult stem cell. Hair follicle stem cells (HFSCs) act as cancer cells of origin for cutaneous squamous cell carcinoma (SCC) and undergo defined cycles of quiescence and activation. The data presented here show that HFSCs are unable to initiate tumors during the quiescent phase of the hair cycle, indicating that the mechanisms that keep HFSCs dormant are dominant to the gain of oncogenes (Ras) or the loss of tumor suppressors (p53). Furthermore, Pten activity is necessary for quiescence based tumor suppression, as its deletion alleviates tumor suppression without affecting proliferation. These data demonstrate that stem cell quiescence is a form of tumor suppression in HFSCs, and that Pten plays a role in maintaining quiescence in the presence of tumorigenic stimuli. This experiment includes RNA profiling of hair follicle stem cells at various stages of tumorigenesis
Stem cell quiescence acts as a tumour suppressor in squamous tumours.
Specimen part
View SamplesIn many organs, adult stem cells are uniquely poised to serve as cancer cells of origin. In the epidermis, hair follicle stem cells (HFSCs) cycle through stages of quiescence (telogen) and proliferation (anagen) to drive hair growth. Within the hair follicle, HFSCs are capable of initiating squamous cell carcinoma, yet it is unclear how the hair cycle contributes to tumorigenesis. The data presented here show that HFSCs are unable to initiate tumors during the quiescent phase of the hair cycle, indicating that the mechanisms that keep HFSCs dormant are dominant to gain of oncogenes (Ras) or loss of tumor suppressors (p53). Instead, prolonged oncogenic stimuli only exert their effects when HFSC quiescence mechanisms are removed by normal HFSC activation. Furthermore, Pten activity is necessary for quiescence based tumor suppression, since Pten deletion alleviates this stem cell specific ability without affecting proliferation per se. Overall design: Small RNAs were cloned from Trizol-lysed cells sorted from mouse skin and sequenced with the Illumina HiSeq2000.
Stem cell quiescence acts as a tumour suppressor in squamous tumours.
No sample metadata fields
View Samples