Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA289931 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression data from xenograft in BALB/c 6-wk-old nude mice with PC3 prostate cancer cells stably expressing PML or a vector control after treatment of the mice with palbociclib (100mg/kg/day diluted in sodium lactate 50mM pH4 given by gavage) during 5 consecutive days PML plays a role in the senescence tumor suppressor response of normal cells to oncogenic stress. PML also mediates therapy-induced senescence in acute promyelocytic leukemia cells after treatment with retinoic acid. However, many tumor cell lines fail to engage a complete senescence response to PML activation. Interestingly, in vivo and in vitro combination of PML overexpression with CDK inhibition induce senescence in PC3 prostate cancer cells. We used microarray to characterize the gene expression profile of PC3 stably expressing PML or a control vector after subcutaneous injection in BALB/c 6-wk-old nude mice and treatment of the mice with palbociclib (100mg/kg/day) during 5 consecutive days.. PC3 cells were infected with a retroviral vector that express PML or an empty vector before subcutaneous injection of 10^6 cells in both flanks of BALB/c 6-wk-old nude mice. Then, mice were treated for 5 consecutive days with palbociclib (100mg/kg/day diluted in sodium lactate 50mM pH4 given by gavage)
2016-07-03 | E-GEOD-70923 | biostudies-arrayexpress
Project description:Expression data from xenograft in BALB/c 6-wk-old nude mice with PC3 prostate cancer cells stably expressing PML or a vector control after treatment of the mice with palbociclib (100mg/kg/day diluted in sodium lactate 50mM pH4 given by gavage) during 5 consecutive days PML plays a role in the senescence tumor suppressor response of normal cells to oncogenic stress. PML also mediates therapy-induced senescence in acute promyelocytic leukemia cells after treatment with retinoic acid. However, many tumor cell lines fail to engage a complete senescence response to PML activation. Interestingly, in vivo and in vitro combination of PML overexpression with CDK inhibition induce senescence in PC3 prostate cancer cells. We used microarray to characterize the gene expression profile of PC3 stably expressing PML or a control vector after subcutaneous injection in BALB/c 6-wk-old nude mice and treatment of the mice with palbociclib (100mg/kg/day) during 5 consecutive days..
2016-01-01 | GSE70923 | GEO
Project description:Subcutaneous xenografts were derived utilizing either PC3 cells engineered to stably overexpress MAOA or empty vector controls in mice receiving docetaxel treatment. Tumor gene expression was profiled using Agilent gene expression microarrays. Custom Agilent 44K whole human genome expression oligonucleotide microarrays were used to profile subcutaneous xenograft tumors derived utilizing either PC3 cells engineered to stably overexpress MAOA or empty vector controls in mice receiving docetaxel treatment. Total RNA was isolated and amplified prior to hybridization against a common reference pool of prostate tumor cell lines.
2014-07-03 | E-GEOD-53944 | biostudies-arrayexpress
Project description:RNA was isolated from ectopically sFRP1-expressing MDA-MB-231 cells and control MDA-MB-231 cells and as well from tumor lysates arising from these cells as nude mouse xenograft. Gene expression profiles for these samples were investigated using Affymetrix arrays. Experiment Overall Design: MDA-MB-231 human breast cancer cells were stably transfected with human sFRP1 encoding vector or empty vector as control. After the selection with antibiotics, three clones of MDA-MB-231/sFRP1 and three clones of MDA-MB-231/control were selected. These six clones were cultured individually in DMEM 10% FCS with 1mg/ml G-418. When cells reached 70-80% confluence, RNA was isolated from the cells. In parallel, the three clones of MDA-MB-231/sFRP1 and the three clones of MDA-MB-231/control were pooled respectively. One million of cells from each pool were suspended in 100ul PBS and injected to fat pads of female balb/c nude mice (6 mice were injected with MDA-MB-231/sFRP1 and 5 mice were injected with MDA-MB-231/control) to do a xenograft experiment. A few - several weeks after, mice were sacrificed when tumor reached a certain size, tumors were taken and RNA was isolated using trizol reagent.
2009-05-11 | E-GEOD-13806 | biostudies-arrayexpress
Project description:Subcutaneous xenografts were derived utilizing either PC3 cells engineered to stably overexpress MAOA or empty vector controls in mice receiving docetaxel treatment. Tumor gene expression was profiled using Agilent gene expression microarrays.
2014-07-03 | GSE53944 | GEO
Project description:0.9x10^11 vg of AAV6.2 vectors containing the murine Il13 cDNA were administered intratracheally to Balb/c mice (9-12 wk). As a control, AAV6.2 vectors containing non-coding “stuffer DNA” were used. To assess vector-mediated effects following AAV6.2 administration, expression in AAV-stuffer treated animals was further compared to mice treated with PBS.
2015-05-31 | E-MTAB-2598 | biostudies-arrayexpress
Project description:Human HCC cell line, MHCC-97L, was subcutaneously injected to BALB/c nude mice. Two weeks post injection, mice were randomised to receive vehicle or PIM447 (60mg/kg) by oral gavage three times a week for two weeks. Total RNA was extracted from the tumor xenograft (Vehicle, n=2; PIM447, n=2) and subjected to RNA sequencing. Expression profiling of the tumors between vehicle control and PIM447 treated groups was compared.
2020-06-03 | GSE142871 | GEO
Project description:TMT proteomics was used to detect the difference in protein expression of bevacizumab-resistant xenograft tumor tissue in nude mice.
2022-10-13 | PXD030202 | Pride
Project description:Transcriptomic studies of human tumor xenografts are complicated by the presence of murine cellular mRNA. As such, it is useful to know the extent to which mouse mRNA cross-hybridizes to any given array platform. In this study, murine cDNA samples from diverse sources were hybridized to Affymetrix Human Genome U133 Plus 2.0 Arrays. In this regard it is possible to identify specific probes that are potential targets of cross-species interference. Array data was generated for 5 different mouse cDNAs and 5 different human cDNAs hybridized to human Affymetrix U133 Plus 2 arrays [3 replicates for each biological sample]. Samples included A) mouse and B) human universal RNA (Strategene, La Jolla, CA), C) B16F10 murine melanoma tumor and D) skin from same model [C57BL/6 mice] E) COLON-26 murine tumor xenograft and F) skin from same model [Balb/C mice] G) NCI-H522 human lung carcinoma xenograft and H) skin from same model (nude mice) I) LOX-IMVI human melanoma xenograft and J) skin from same model (nude mice).
2013-07-31 | E-GEOD-49353 | biostudies-arrayexpress
Project description:Background: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors worldwide, with unclear pathogenesis. Sphingomyelin phodiesterase acid-like 3A (SMPDL3A) affects cell differentiation and participates in immune regulation. However, its molecular biological function in HCC has not yet been elucidated. Methods：Data from 180 HCC patients were analyzed the relationship between the expression of SMPDL3A in liver cancer tissues and the prognosis of liver cancer patients. Crispr-Cas9 dual vector lentivirus was used to knock out SMPDL3A in HCC cell lines. The effects of SMPDL3A on cell viability were determined by CCK8 assay, clone formation experiment, cell cycle assay, cell scratch, TUNEL experiment and flow cytometry. Xenograft tumor assays in BALB/c nude mice confirmed that SMPDL3A promoted tumor growth and in vivo. Preliminary exploration of SMPDL3A interacting protein by mass spectrometry analysis and co-immunoprecipitation. Results: This study showed that the expression of SMPDL3A in HCC tissue differed from that in tumor-adjacent tissues. Moreover, the overall survival rate and tumor-free survival rate of patients with high-SMPDL3A expression were significantly lower than those with low-SMPDL3A expression. SMPDL3A expression was closely related to the level of protein induced by PIVKA-II, liver cirrhosis, tumor diameter, microvascular invasion, and Barcelona clinic liver cancer staging. Thus, SMPDL3A is an independent risk factor that affects the tumor-free survival rate and overall survival rate of HCC patients. In vitro study using Crispr-Cas9 genome editing technology revealed the knockout effect of SMPDL3A on cell proliferation, apoptosis, and migration. Cell counting kit-8 assay and clone formation experiment showed that sgSMPDL3A inhibited tumor cell proliferation and migration. Flow cytometry and TUNEL assay showed that sgSMPDL3A promoted apoptosis in tumors. Moreover, sgSMPDL3A inhibited tumor growth during subcutaneous tumor formation in nude mice. Immunohistochemistry of Ki67 and PNCA also indicated that sgSMPDL3A inhibited subcutaneous tumor proliferation in tumor-bearing nude mice. Further experiments showed that SMPDL3A interacts with the enhancer of rudimentary homolog (ERH). Conclusions: High-SMPDL3A expression was related to poor prognosis of patients with HCC. Knockout of SMPDL3A inhibited the proliferation and migration and accelerated the migration of HCC cells. SMPDL3A interacted with ERH to affect the tumorigenesis and progression of HCC.
2022-05-23 | PXD032824 | Pride