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accession-icon GSE32911
Compound C prevents the unfolded protein response during glucose deprivation through a mechanism independent of AMPK and BMP signaling.
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Inhibiting the unfolded protein response (UPR) can be a therapeutic approach, especially for targeting the tumor microenvironment. We found that compound C (also known as dorsomorphin) prevented the UPR and exerted enhanced cytotoxicity during glucose deprivation. The UPR-inhibiting activity of compound C was not associated with either AMPK or BMP signaling inhibition.

Publication Title

Compound C prevents the unfolded protein response during glucose deprivation through a mechanism independent of AMPK and BMP signaling.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE16157
Mitochondria regulate the unfolded protein response leading to cancer cell survival under glucose deprivation conditions
  • organism-icon Homo sapiens
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Cancer cells consume large amounts of glucose because of their specific metabolic pathway. However, cancer cells exist in tumor tissue where glucose is insufficient. To survive, cancer cells likely have the mechanism to elude their glucose addiction. Here we show that functional mitochondria are essential if cancer cells are to avoid glucose addiction.

Publication Title

Mitochondria regulate the unfolded protein response leading to cancer cell survival under glucose deprivation conditions.

Sample Metadata Fields

Disease, Cell line, Time

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accession-icon GSE13548
Expression data from human cancer cells treated with UPR modulators under ER stress conditions
  • organism-icon Homo sapiens
  • sample-icon 40 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The unfolded protein response (UPR) is a cellular defense mechanism against glucose deprivation, a cell condition that occurs in solid tumors.

Publication Title

Chemical genomics identifies the unfolded protein response as a target for selective cancer cell killing during glucose deprivation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE80320
Mitochondrial deficiency impairs hypoxic induction of HIF-1 transcriptional activity and retards tumor growth
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Mitochondria can be involved in regulating cellular stress response to hypoxia and tumor growth, but little is known about that mechanistic relationship. Here, we show that mitochondrial deficiency severely retards tumor xenograft growth with impairing hypoxic induction of HIF-1 transcriptional activity. Using mtDNA-deficient rho0 cells, we found that HIF-1 pathway activation was comparable in slow-growing rho0 xenografts and rapid-growing parental xenografts. Interestingly, we found that ex vivo rho0 cells derived from rho0 xenografts exhibited slightly increased HIF-1alpha expression and modest HIF-1 pathway activation regardless of oxygen concentration. Surprisingly, rho0 cells, as well as parental cells treated with oxidative phosphorylation inhibitors, were unable to boost HIF-1 transcriptional activity during hypoxia, although HIF-1alpha protein levels were ordinarily increased in these cells under hypoxic conditions. These findings indicate that mitochondrial deficiency causes loss of hypoxia-induced HIF-1 transcriptional activity and thereby might lead to a constitutive HIF-1 pathway activation as a cellular adaptation mechanism in tumor microenvironment.

Publication Title

Mitochondrial deficiency impairs hypoxic induction of HIF-1 transcriptional activity and retards tumor growth.

Sample Metadata Fields

Cell line

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accession-icon SRP062555
Global analysis of pre-mRNA subcellular localization upon splicing inhibition by spliceostatin A
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

RNA-Seq analysis of SSA treated cells Overall design: HeLa cells, nuclear and cytoplasmic fractions, treated with SSA or MeOH

Publication Title

Global analysis of pre-mRNA subcellular localization following splicing inhibition by spliceostatin A.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE44356
Expression data from wild-type and HMGN1 knockout mice injected with N-nitrosodiethylamine
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

HMGN1 contributes to the shortened latency of liver tumorigenesis by changing a chromatin structure and expression of relevant genes

Publication Title

Loss of the nucleosome-binding protein HMGN1 affects the rate of N-nitrosodiethylamine-induced hepatocarcinogenesis in mice.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE24783
Gene profiling of the cell death induced by heat stress in HSC-3 human oral squamous carcinoma cells
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Hyperthermia is widely used to treat patients with various cancers. The 42.5C is well known as inflection point of hyperthermia and generally up to 42C of hyperthermia is used in clinical case to combine with other therapy. Here, the effects of heat stress at 42 or 44C for 90 min on the gene expression in HSC-3 human oral squamous carcinoma cells were investigated using an Affymetrix GeneChip system. The cells were treated with heat stress (42 or 44C for 90 min) and followed by incubation for 0, 6, or 12 h at 37C. The percentage of cell death was 5.0 1.5 (mean SD) at 42C for 12 h and 17.4 0.6 at 44C for 12 h. Of approximately 47,000 probe sets analyzed, many genes that were differentially expressed by a factor 2.0 or greater were identified in the cells treated with heat stress at 42 and 44C.

Publication Title

Gene networks related to the cell death elicited by hyperthermia in human oral squamous cell carcinoma HSC-3 cells.

Sample Metadata Fields

Cell line, Treatment, Time

View Samples
accession-icon GSE55687
Expression data of mouse embyonic fibroblasts established from Phgdh KO embryos (KO-MEFs) cultured with or without L-Ser
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

L-Ser deficiency leads to growth arrest, tissue malformation and embryonic lethality in mice. However, the molecular mechanism by which L-Ser deficiency impairs basic cellular function remains largely unexplored.

Publication Title

Microarray data on altered transcriptional program of Phgdh-deficient mouse embryonic fibroblasts caused by ʟ-serine depletion.

Sample Metadata Fields

Specimen part

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accession-icon SRP012147
Alkbh1/Tzfp Repress a Non-Repeat piRNA Cluster in Pachytene Spermatocytes
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

Piwi proteins and Piwi-interacting small RNAs (piRNAs) have known functions in transposon silencing in the male germline of fetal and newborn mice. Both are also necessary for spermatogenesis in adult testes, however, their function here remains a mystery. Here, we use germ cell isolations and small RNA sequencing to show that most piRNAs in meiotic spermatocytes originate from clusters in intergenic non-repeat regions of DNA. The regulation of these piRNA clusters, including the processing of the precursor transcripts into individual piRNAs, is accomplished through mostly unknown processes. We present evidence for a regulatory mechanism for one such cluster, named cluster 1082B, located on chromosome 7 in the mouse genome, containing 788 unique piRNAs. The precursor transcript and individual piRNAs within the cluster are repressed by the Alkbh1 dioxygenase and the transcription repressor Tzfp, which are believed to be interaction partners in testis. We observe more than a thousand-fold upregulation of individual piRNAs in pachytene spermatocytes isolated from Alkbh1-/- and TzfpGTi/GTi testes. Repression is further supported by the identification of a 10 bp Tzfp recognition sequence contained within the precursor transcript. Downregulation of long interspersed elements 1 (LINE1) and intracisternal A-particle (IAP) transcripts in the Alkbh1-/- and TzfpGTi/GTi testes leads us to propose a potential role for the 1082B-encoded piRNAs in transposon silencing. Overall design: Characterization of small RNAs in mouse pachytene spermatocytes for wild-type (WT) and Alkbh1-/- and TzfpGTi/GTi, and mRNA in mouse pachytene spermatocytes for wild-type (WT) and Alkbh1-/-

Publication Title

Alkbh1 and Tzfp repress a non-repeat piRNA cluster in pachytene spermatocytes.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE66074
Effects of the histone demethylase LSD1/KDM1A on the gene expression program of murine hematopoietic progenitor cells.
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We established transgenic mice overexpressing the histone demethyase LSD1/KDM1A under the control of Sca-1 promoter and investigated the global changes in gene expression in hematopoietic progenitor cells using a microarray-

Publication Title

Overexpression of the shortest isoform of histone demethylase LSD1 primes hematopoietic stem cells for malignant transformation.

Sample Metadata Fields

Specimen part

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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