Unexpected growth-promoting effect of oxaliplatin in ERCC1-transfected human colon cancer cells
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ABSTRACT:
PROVIDER: PRJNA433682 | ENA |
REPOSITORIES: ENA
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Project description:The nucleotide excision repair protein ERCC1 has been repeatedly shown to be involved in the sensitivity of cancer cells to platinum derivatives. In order to better understand this process, we transfected HCT-116 cells with a plasmid encoding ERCC1 and studied their in vitro and in vivo behaviour. The Trop2 protein was identified as being potentially involved in the underlying mechanism for these observations. Our results suggest complex regulation of signalling in cancer cells exposed to cancer drugs.
2018-02-10 | GSE110425 | GEO
Project description:Although it is clear that probiotics improve intestinal barrier function, little is known about the effects of probiotics on the aging intestine. We investigated effects of 10-wk bacterial supplementation of Lactobacillus plantarum WCFS1, Lactobacillus casei BL23, or Bifidobacterium breve DSM20213 on gut barrier and immunity in 16-week-old accelerated aging Ercc1-/Δ7 mice, which have a median lifespan of ~20wk, and their wild-type littermates. The colonic barrier in Ercc1-/Δ7 mice was characterized by a thin (<10µm) mucus layer. L. plantarum prevented this decline in mucus integrity in Ercc1-/Δ7 mice, whereas B. breve exacerbated it. Bacterial supplementations affected the expression of immune-related genes, including Toll-like receptor 4. Regulatory T cell frequencies were increased in the mesenteric lymph nodes of L. plantarum- and L. casei-treated Ercc1-/Δ7 mice. L. plantarum- and L. casei-treated Ercc1-/Δ7 mice showed increased specific antibody production in a T cell-dependent immune response in vivo. By contrast, the effects of bacterial supplementation on wild-type control mice were negligible. Thus, supplementation with L. plantarum – but not with L. casei and B. breve – prevented the decline in the mucus barrier in Ercc1-/Δ7 mice. Our data indicate that age is an important factor influencing beneficial or detrimental effects of candidate probiotics. These findings also highlight the need for caution in translating beneficial effects of probiotics observed in young animals or humans to the elderly.
2016-10-19 | GSE87368 | GEO
Project description:Aim: mRNA profile of HCT116 human colon cancer cells to study the early response of cells to oxaliplatin exposure at low doses (0.5µM) Results: After treatment with oxaliplatin for 24h at 0.5µM, only a very small fraction of genes were mis-regulated. They fall mainly include P53-response genes, genes regulating inflammation, or genes regulating cytoskeleton.
2023-03-20 | GSE227315 | GEO
Project description:Transcriptome analysis of epididymal white adipose tissue (WAT) depots in Ercc1 animals: To further elucidate the role of ERCC1 in WAT we scanned the transcriptome of 15 day old wt and Ercc1 epididymal WAT.
2013-11-04 | E-MEXP-3930 | biostudies-arrayexpress
Project description:Background: Several genetic defects of the nucleotide excision repair (NER) pathway, including deficiency of the Excision Repair Cross-Complementing rodent repair deficiency, complementation group 1 (ERCC1), result in pre-mature aging, impaired growth, microcephaly and delayed development of the cerebellum. Such a phenotype also occurs in ERCC1-knockout mice which survive for up to 4 weeks after birth. Therefore, we analyzed cerebellar and hippocamapal transcriptomes of these animals at 3 weeks of age to identify the candidate mechanisms underlying brain consequences of reduced ERCC1 activity. Results: In the cerebellum, the most prominent change was upregulation of genes that are associated with gliosis. Although Purkinje cell degeneration has been reported in some mouse strains with NER impairment, Purkinje cell transcriptome was mostly unaffected by the ERCC1 knockout. In the hippocampus, the gliosis response was minimal. Instead, there was an extensive downregulation of genes related to lipid metabolism including several enzymes of the cholesterol biosynthesis pathway as well as lipoproteins and plasma membrane proteins. Reduced expression of the cholesterol biosynthesis pathway genes was also present in the neocortex of adult mice whose ERCC1 gene was replaced by a mutant allele with a partial activity. Conclusions: Downregulation of forebrain cholesterol biosynthesis genes is a newly identified consequence of ERCC1 deficiency. Its presence in adult mice suggests that it is not a secondary consequence of brain growth impairment. Instead, reduced cholesterol biosynthesis may contribute to such an impairment as well as affect function of mature synapses.
2011-08-16 | GSE31199 | GEO
Project description:The XPF-ERCC1 endonuclease is required for repair of helix-distorting DNA damage and interstrand crosslinks. Here we have engineered a severe mutation in Ercc1 gene (in which the last 7 amino acids are missing; named as "Ercc1-delta") leading to extreme sensitivity to DNA crosslinks and progeria.To investigate whether a disturbance in growth and metabolism could explain the pronounced accelerated organismal deterioration seen in Ercc1 delta mice, we evaluated the liver transcriptome of 16-week-old wt and mutant mice (n=6). At this age, the Ercc1-delta mice have not yet become cachectic.
2008-06-01 | E-MEXP-1503 | biostudies-arrayexpress
Project description:Total RNA was isolated from wt and Ercc1-/- pancreata from 15 days old C57BL/6J wt and Ercc1-/- mice
2021-05-15 | E-MTAB-10393 | biostudies-arrayexpress
Project description:To identify key drivers of oxaliplatin resistance, we collected and analyzed the DEGs between oxaliplatin-resistant and oxaliplatin-non-resistant patient samples
2023-02-28 | GSE206501 | GEO
Project description:Using these samples, it has been shown that the transcriptional landscape in glomeruli of Ercc1[-/Δ] mice at a rather young age of 14 weeks mimics that of mice which have undergone real-life renal aging. Thus, young Ercc1[-/Δ] mice can be used as a model system for glomerular aging in future studies.
2012-12-21 | GSE43061 | GEO
Project description:Background: Several genetic defects of the nucleotide excision repair (NER) pathway, including deficiency of the Excision Repair Cross-Complementing rodent repair deficiency, complementation group 1 (ERCC1), result in pre-mature aging, impaired growth, microcephaly and delayed development of the cerebellum. Such a phenotype also occurs in ERCC1-knockout mice which survive for up to 4 weeks after birth. Therefore, we analyzed cerebellar and hippocamapal transcriptomes of these animals at 3 weeks of age to identify the candidate mechanisms underlying brain consequences of reduced ERCC1 activity. Results: In the cerebellum, the most prominent change was upregulation of genes that are associated with gliosis. Although Purkinje cell degeneration has been reported in some mouse strains with NER impairment, Purkinje cell transcriptome was mostly unaffected by the ERCC1 knockout. In the hippocampus, the gliosis response was minimal. Instead, there was an extensive downregulation of genes related to lipid metabolism including several enzymes of the cholesterol biosynthesis pathway as well as lipoproteins and plasma membrane proteins. Reduced expression of the cholesterol biosynthesis pathway genes was also present in the neocortex of adult mice whose ERCC1 gene was replaced by a mutant allele with a partial activity. Conclusions: Downregulation of forebrain cholesterol biosynthesis genes is a newly identified consequence of ERCC1 deficiency. Its presence in adult mice suggests that it is not a secondary consequence of brain growth impairment. Instead, reduced cholesterol biosynthesis may contribute to such an impairment as well as affect function of mature synapses. We analyzed the hippocampus and cerebellum from three Ercc1-/- and three WT littermates using the Affymetrix Mouse Genome 430_2.0. Data was analyzed using the dChip DNA-Chip analyzer software .
2011-08-15 | E-GEOD-31199 | biostudies-arrayexpress