Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA290632 | ENA |
REPOSITORIES: ENA
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Project description:The cell differentiation potential of 13-cis retinoic acid (RA) has not succeeded in the clinical treatment of glioblastoma (GBM) so far. However, RA may also induce the expression of disistance genes such as HOXB7 which can be suppressed by Thalidomide (THAL). Therefore, we tested if combined treatment with RA+THAL may inhibit growth of glioblastoma in vivo. Treatment with RA+THAL but not RA or THAL alone significantly inhibited tumour growth. The synergistic effect of RA and THAL was corroborated by the effect on proliferation of glioblastoma cell lines in vitro. HOXB7 was not upregulated but microarray analysis validated by real-time PCR identified four potential resistance genes (IL-8, HILDPA, IGFBPA, and ANGPTL4) whose upregulation by RA was suppressed by THAL. Furthermore, genes coding for small nucleolar RNAs (snoRNA) were identified as a target for RA for the first time, and their upregulation was maintained after combined treatment. Pathway analysis showed upregulation of the Ribosome pathway and downregulation of pathways associated with proliferation and inflammation. Combined treatment with RA + THAL delayed growth of GBM xenografts and suppressed putative resistance genes associated with hypoxia and angiogenesis. This encourages further pre-clinical and clinical studies of this drug combination in GBM. The purpose was to study differential gene expression in glioblastoma xenografts after treatment with 13-cis retinoic acid (RA), thalidomide (Thal) or a combination of both drugs.
2015-07-23 | E-GEOD-71224 | biostudies-arrayexpress
Project description:The cell differentiation potential of 13-cis retinoic acid (RA) has not succeeded in the clinical treatment of glioblastoma (GBM) so far. However, RA may also induce the expression of disistance genes such as HOXB7 which can be suppressed by Thalidomide (THAL). Therefore, we tested if combined treatment with RA+THAL may inhibit growth of glioblastoma in vivo. Treatment with RA+THAL but not RA or THAL alone significantly inhibited tumour growth. The synergistic effect of RA and THAL was corroborated by the effect on proliferation of glioblastoma cell lines in vitro. HOXB7 was not upregulated but microarray analysis validated by real-time PCR identified four potential resistance genes (IL-8, HILDPA, IGFBPA, and ANGPTL4) whose upregulation by RA was suppressed by THAL. Furthermore, genes coding for small nucleolar RNAs (snoRNA) were identified as a target for RA for the first time, and their upregulation was maintained after combined treatment. Pathway analysis showed upregulation of the Ribosome pathway and downregulation of pathways associated with proliferation and inflammation. Combined treatment with RA + THAL delayed growth of GBM xenografts and suppressed putative resistance genes associated with hypoxia and angiogenesis. This encourages further pre-clinical and clinical studies of this drug combination in GBM.
2015-07-23 | GSE71224 | GEO
Project description:We performed pulldown assays followed by mass-spectrometry analysis using biotin-tagged 13-cis retinoic acid to identify its binding targets in HeLa cells
2022-01-14 | PXD029579 | Pride
Project description:13-cis retinoic acid treatment of human sebocytes (SEB-1)
| PRJNA108917 | ENA
Project description:This study compared the gene expression change of glioblastoma stem-like cells before and after retinoic acid treatment Glioblastoma neurospheres 10627 and 20913 were treated with retinoic acid for 8h and 48h and compared with control
2011-04-06 | E-GEOD-21336 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series:; GSE10432: 13-cis retinoic acid treatment of human sebocytes (SEB-1); GSE10433: Human Skin: Before and 1 week after Isotretinoin Treatment; The pathogenesis of acne has been linked to multiple factors such as increased sebum production, inflammation, follicular hyperkeratinization, and the action of Propionibacterium acnes within the follicle. 13-cis Retinoic Acid (13-cis RA, isotretinoin) is the most potent agent in acne treatment. Surprisingly, its mechanism of action in acne is still unknown. Gene expression profiling of cultured human immortalized sebocytes (SEB-1) treated with 13-cis RA was performed to gain insights into its sebocyte-specific mechanism of action. SEB-1 sebocytes were cultured with 0.1 uM 13-cis RA for 72 hours or vehicle control. Gene array expression profiling was conducted using Affymetrix HG-U95Av2 arrays in order to examine changes in gene expression as a result of treatment. A total of 85 genes (78 different genes) were significantly influenced by 13-cis RA: 58 were upregulated and 27 were down-regulated. There were changes in several genes involved in apoptosis and innate immunity. These studies are the first describing the sebocyte- specific response in gene expression associated with isotretinoin therapy and are valuable in identifying potential therapeutic targets in acne. The pathogenesis of acne has been linked to multiple factors such as increased sebum production, inflammation, follicular hyperkeratinization, and the action of Propionibacterium acnes within the follicle. 13-cis Retinoic Acid (13-cis RA, isotretinoin) is the most potent agent in acne treatment. Surprisingly, its mechanism of action in acne is still unknown. Gene expression profiling of skin from 6 patients treated with isotretinoin was performed to gain insights into its mechanism of action. Skin biopsies were obtained from the patients at baseline and at one-week isotretinoin treatment. Gene array expression profiling was conducted using Affymetrix HG-U133A 2.0 arrays in order to examine changes in gene expression as a result of treatment. After treatment, 43 genes were significantly changed: 38 up-regulated and 5 down-regulated. A significant proportion of these genes are involved in pathways that regulate differentiation, tumor suppression, serine proteases, serine protease inhibitors and solute transfer. These studies are the first describing the initial changes in gene expression associated with isotretinoin therapy and are valuable in identifying potential therapeutic targets in acne. Experiment Overall Design: Refer to individual Series
2008-04-06 | E-GEOD-10434 | biostudies-arrayexpress
Project description:Gene expression data from BE(2)-C cells treated in triplicate with either vehicle (DMSO), 5 M-NM-<M all-trans retinoic acid (ATRA), 1 mM valproic acid (VPA), or 5 M-NM-<M ATRA + 1 mM VPA for 6, 24, or 72 hours. Genome-wide expression profiling was performed using Affymetrix U133A microarrays. While cytotoxic chemotherapy remains the hallmark of cancer treatment, intensive regimens fall short in many malignancies, including high-risk neuroblastoma. One alternative strategy is to therapeutically promote tumor differentiation. We created a gene expression signature to measure neuroblast maturation, adapted it to a high-throughput platform, and screened a diversity oriented synthesis-generated small-molecule library for differentiation inducers. We identified BRD8430, containing a nine-membered lactam, an ortho-amino anilide functionality, and three chiral centers, as a selective Class I histone deacetylase (HDAC) inhibitor (HDAC1 > 2 > 3). Further investigation demonstrated that selective HDAC1/HDAC2 inhibition using compounds or RNA interference induced differentiation and decreased viability in neuroblastoma cell lines. Combined treatment with 13-cis retinoic acid augmented these effects and enhanced activation of retinoic acid signaling. Therefore, by applying a chemical genomic screening approach we identified selective HDAC1/HDAC2 inhibition as a strategy to induce neuroblastoma differentiation. BE(2)-C cells were treated in triplicate with either vehicle (DMSO), 5 M-NM-<M all-trans retinoic acid (ATRA), 1 mM valproic acid (VPA), or 5 M-NM-<M ATRA + 1 mM VPA for 6, 24, or 72 hours. Genome-wide expression profiling was performed using Affymetrix U133A microarrays [HT-HG_U133A Early Access].
2013-04-08 | E-GEOD-45587 | biostudies-arrayexpress
Project description:Gene expression data from BE(2)-C cells treated in triplicate with either vehicle (DMSO), 5 μM all-trans retinoic acid (ATRA), 1 mM valproic acid (VPA), or 5 μM ATRA + 1 mM VPA for 6, 24, or 72 hours. Genome-wide expression profiling was performed using Affymetrix U133A microarrays. While cytotoxic chemotherapy remains the hallmark of cancer treatment, intensive regimens fall short in many malignancies, including high-risk neuroblastoma. One alternative strategy is to therapeutically promote tumor differentiation. We created a gene expression signature to measure neuroblast maturation, adapted it to a high-throughput platform, and screened a diversity oriented synthesis-generated small-molecule library for differentiation inducers. We identified BRD8430, containing a nine-membered lactam, an ortho-amino anilide functionality, and three chiral centers, as a selective Class I histone deacetylase (HDAC) inhibitor (HDAC1 > 2 > 3). Further investigation demonstrated that selective HDAC1/HDAC2 inhibition using compounds or RNA interference induced differentiation and decreased viability in neuroblastoma cell lines. Combined treatment with 13-cis retinoic acid augmented these effects and enhanced activation of retinoic acid signaling. Therefore, by applying a chemical genomic screening approach we identified selective HDAC1/HDAC2 inhibition as a strategy to induce neuroblastoma differentiation.
2013-04-08 | GSE45587 | GEO
Project description:Transcriptomic analysis of Retinoic acid and 9 cis retinoic acid in zebrafish.
| PRJNA176664 | ENA
Project description:We examined the effects of all-trans-retinoic acid and 9-cis-retinoic acid on gene expression in Mel202 uveal melanoma cells
2025-03-15 | GSE149445 | GEO