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ABSTRACT: p53 in colorectal cancer cells

OTHER RELATED OMICS DATASETS IN: GSE67110PXD001976MSV000079767

PROVIDER: PRJNA278966 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1920910.fastq.gz	Fastqsanger.gz
	SRR1920911.fastq.gz	Fastqsanger.gz
	SRR1925761.fastq.gz	Fastqsanger.gz
	SRR1920912.fastq.gz	Fastqsanger.gz
	SRR1925762.fastq.gz	Fastqsanger.gz

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Extracts from sweet sorghum (Sorghum bicolor), a feedstock for biorefining, suppressed proliferation and elevated apoptosis in human colon cancer stem cells via suppression of Wnt/beta-catenin signaling pathway

Project description:In colorectal cancer, p53 is commonly inactivated, associated with chemo-resistance, and marks the transition from non-invasive to invasive disease. Cancers, including colorectal cancer, are thought to be diseases of aberrant stem cell populations, as stem cells are able to self-renew, making them long-lived enough to acquire mutations necessary to manifest the disease. We have shown that extracts from sweet sorghum stalk components eliminate colon cancer stem cells (CCSC) in a partial p53-dependent fashion. However, the underlying mechanisms are unknown. In the present study, CCSC were transfected with short hairpin-RNA against p53 (CCSC p53 shRNA) and treated with sweet sorghum phenolics extracted from different plant components (dermal layer, leaf, seed head and whole plant). While all components demonstrated anti-proliferative and pro-apoptotic effects in CCSC, phenolics extracted from the dermal layer and seed head were more potent in eliminating CCSC by elevating caspases 3/7 activity, PARP cleavage, and DNA fragmentation in a p53-dependent and p53-independent fashion, respectively. Further investigations revealed that the anti-proliferative and pro-apoptotic effects were associated with decreases in beta-catenin protein levels, and beta-catenin targets cyclin D1, cMyc, and survivin. These results suggest that the anti-proliferative and pro-apoptotic effects of sweet sorghum extracts against human colon cancer stem cells are via suppression of Wnt/beta-catenin pro-survival signaling in a p53-dependent (dermal layer) and partial p53-independent (seed head) fashion. LCMS used to identify phenolic compounds associated with extract activity

2014-05-01 | MTBLS69 | MetaboLights

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Project description:Genome-wide p53-occupancy in colorectal cancer cells.

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Integrated Analysis of Genes Encoding ATP-Dependent Chromatin Remodelers Identifies CHD7 as a Potential Target for Colorectal Cancer Therapy

Project description:We experimentally demonstrated that CHD7 promotes the growth of colorectal cancer cells in vitro and in vivo. Mechanistically, RNA-seq and ATAC-seq approaches together with ChIP assays indicated that CHD7 can bind to the promoters of target genes to maintain chromatin accessibility and facilitate transcription. We found that CHD7 knockdown downregulates AK4 expression and activates AMPK phosphorylation, thereby promoting the phosphorylation and stability of p53 and leading to the inhibition of the colorectal cancer growth. Our genomic analyses of ATPCRs across large-scale cancer specimens identified potential therapeutic targets and our experimental studies revealed a novel CHD7-AK4-AMPK-p53 axis that plays an oncogenic role in colorectal cancer.

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LINC01021 attenuates expression and affects alternative splicing of a subset of p53-regulated genes

Project description:Loss of the p53-inducible LINC01021 in p53-proficient CRC cell lines results in increased sensitivity to DNA-damaging chemotherapeutics. Here, we comprehensively analyzed how LINC01021 affects the p53-induced transcriptional program. Using a CRISPR/Cas9-approach we deleted the p53 binding site in the LINC01021 promoter of SW480 colorectal cancer cells and subjected them to RNA-Seq analysis after activation of ectopic p53. RNA affinity purification followed by mass spectrometry was used identify proteins associated with LINC01021.

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Cell Context Dependent p53 Genome-Wide Binding Patterns and Enrichment at Repeats

Project description:We mapped the genomic binding sites of the tumor suppressor protein p53 in the human colorectal cancer cell line HCT116 and report here that the binding patterns of endogenous wild type p53 differed significantly between the genomes of the cancer cell line HCT116 and the normal human IMR90 fibroblasts (GSE31558) under the same experimental conditions (6 hr treatment with 5-fluorouracil). p53 binding differences affect promoter regions, CpG islands and major families of human repeat elements such as LTR, LINE and SINE. While p53 genomic binding sites residing in repeats have been reported before, we show here that the fraction of the p53 genomic binding sites residing in different repeat families differs between the normal and cancer human cell lines. We confirm that the p53 genomic binding sites in HCT116 cells are excluded from CpG islands, an observation we made previously based on analysis of data reported by others. While the p53 ability to elicit stress-specific and cell-type-specific responses is well documented, how this specificity is established, at the level of binding to the genome and/or during post-binding events, represents an open question. Our data indicate that p53 binding to the human genome is cell line-specific and highly selective. The differences in the p53 genome-wide binding patterns between the cancer cell line HCT116 and the normal cell line IMR90, namely exclusion from CpG islands and enrichment at repeats in HCT116, likely reflect cancer-associated epigenetic changes in the chromatin. Identification of genomic p53 binding sites in HCT116 cells by ChIP-seq.

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Project description:p53 mutation is common and highly related to radiotherapy resistance in rectal cancer. APR-246, as a small molecule, can restore the tumor-suppressor function to mutant p53. There is no study on combining APR-246 with radiation in rectal cancer; therefore, we examined whether APR-246 sensitized colorectal cancer cells with different p53 status to radiation. The combination treatment had synergistic effects on HCT116p53-R248W/-(p53Mut) cells, followed by HCT116p53+/+(p53WT) cells, and exhibited an additive effect on HCT116p53-/-(p53Null) cells through inhibiting proliferation, enhancing reactive oxygen species, and apoptosis. The results were confirmed in zebrafish xenografts. Comparison of the transcriptome in colorectal cancer cells with different p53 status 72hrs post-treatment with APR-246, irradiation, or the combination of APR-246 with irradiation was carried out. p53Mut and p53WT cells shared more activated pathways and differentially expressed genes following the combination treatment, compared to p53Null cells, although the combination treatment regulated individual pathways in the different cell lines. APR-246 mediated radio-sensitization effects through p53-dependent and -independent ways.

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Expression profiling by p53 status

Project description:Human colorectal carcinoma-derived cell lines, p53 -/-, +/-, +/+ at 0 and 12 hrs after growth arrest. Keywords = p53, expression, colon cancer, CSPG2 Keywords: repeat sample

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Gene expression profiling by miRNA microarray of control and METTL14-overexpressed HT29 human colon cancer cells

Project description:In order to define the cohort of miRNAs whose expression is regulated by METTL14 in p53 mutant colorectal cancer, we constructed HT29 cells stably infected with lentivirus carrying control transfectants (vector) or METTL14 overexpression (METTL14). Subsequently, total RNA was isolated and then performed miRNA Microarray.

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aCGH profiles of parental and oxaliplatin resistant colorectal cancer and ovarian cancer cell lines

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