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Colon cancer cells after escape of late apoptosis [exp_1]

ABSTRACT: In order to explore the potential role of escape of late apoptosis in metastasis, we induced apoptosis and subsequently inhibited the death process in a primary culture of colon cancer cells. Here we wanted to explore the transcriptome of such "undead" cells 7 days after apoptosis induction.

ORGANISM(S): Homo sapiens

PROVIDER: GSE171543 | GEO | 2022/03/08

REPOSITORIES: GEO

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Colon cancer cells after escape of late apoptosis [exp_2]

Project description:In order to explore the potential role of escape of late apoptosis in metastasis, we induced apoptosis and subsequently inhibited the death process in a primary culture of colon cancer cells. Here we wanted to explore the transcriptome of cells treated with the conditioned medium of these surviving cells. Thes cells have been treated for 48h with conditionned media previous RNA extraction and RNAseq.

2022-03-08 | GSE171560 | GEO

Colon cancer cells after escape of late apoptosis

Project description:Colon cancer cells after escape of late apoptosis

| PRJNA720553 | ENA

Colon cancer cells after escape of late apoptosis [exp_2]

Project description:Colon cancer cells after escape of late apoptosis [exp_2]

| PRJNA720091 | ENA

Colon cancer cells after escape of late apoptosis [exp_1]

Project description:Colon cancer cells after escape of late apoptosis [exp_1]

| PRJNA720012 | ENA

Colon cancer cells after escape of late apoptosis

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-03-08 | GSE171679 | GEO

Escape from X inactivation in mouse tissues (RNA-Seq)

Project description:X chromosome inactivation (XCI) silences most genes on one X chromosome in female mammals, but some genes escape XCI. To identify escape gene in vivo and to explore molecular mechanisms that regulate this process we analyzed the allele-specific expression and chromatin structure of X-linked genes in mouse tissues and cells with skewed XCI and distinguishable alleles based on single nucleotide polymorphisms. Using a new method to estimate allelic expression, we demonstrate a continuum between complete silencing and significant expression from the inactive X (Xi). Few genes (2-3%) escape XCI to a significant level and only a minority differs between mouse tissues, suggesting stringent silencing and escape controls. Allelic profiles of DNase I hypersensitivity and RNA polymerase II occupancy of genes on the Xi correlate with escape from XCI. Allelic binding profiles of the DNA binding protein CCCTC-binding factor (CTCF) in different cell types indicate that CTCF binding at the promoter correlates with escape. Importantly, CTCF binding at the boundary between escape and silenced domains may prevent the spreading of active escape chromatin into silenced domains. Examination of allelic expression in mouse hybrid tissues.

2015-02-20 | E-GEOD-59777 | biostudies-arrayexpress

Escape from X inactivation in mouse tissues (ChIP-Seq)

2015-02-20 | E-GEOD-59778 | biostudies-arrayexpress

Tumour-derived exosomes regulate apoptosis of CD45+EpCAM+ cells in lung cancer

Project description:Cancer-derived exosomes can deliver nucleic acids, proteins, and lipids to neighboring or distant cells and subsequently modulate recipient cells. Recently, high levels of microRNAs (miRNAs) have been identified in cancer-derived exosomes, which provide a favorable microenvironment that contribute to tumorigenesis, tumor metastasis, angiogenesis, chemoresistance, and immune escape. Howerer, the mechanism of the cancer-derived exosomes regulating CD45+EpCAM+ cell apoptosis remains unclear.

2022-05-26 | GSE197975 | GEO

Peroxireduxin-4 is over-expressed in colon cancer and its down-regulation leads to apoptosis

Project description:The objective of this study was to gain insights into the biological basis of colon cancer progression by characterizing gene expression differences between normal colon epithelium, corresponding colorectal primary tumors and metastases. We found a close similarity in gene expression patterns between primary tumors and metastases, indicating a correlation between gene expression and morphological characteristics. PRDX4 was identified as highly expressed both in primary colon tumors and metastases, and selected for further characterization. Our study revealed that Prdx4 (PrxIV, AOE372) shows functional similarities to other Prx family members by negatively effecting apoptosis induction in tumor cells. In addition, our studies link Prdx4 with Hif-1M-NM-1, a key regulatory factor of angiogenesis. Targeting Prdx4 may be an attractive approach in cancer therapy, as its inhibition is expected to lead to induction of apoptosis and blockade of Hif-1M-NM-1-mediated tumor angiogenesis. mRNA expression profiling of normal colon epithelium (5), primary colon tumors (12 with 1 replicate) and either lymph node metastases (9 with 2 replicates) or liver metastases (2) and cell lines (4) from twelve colon cancer patients.

2011-06-01 | E-GEOD-26571 | biostudies-arrayexpress

Peroxireduxin-4 is over-expressed in colon cancer and its down-regulation leads to apoptosis

Project description:The objective of this study was to gain insights into the biological basis of colon cancer progression by characterizing gene expression differences between normal colon epithelium, corresponding colorectal primary tumors and metastases. We found a close similarity in gene expression patterns between primary tumors and metastases, indicating a correlation between gene expression and morphological characteristics. PRDX4 was identified as highly expressed both in primary colon tumors and metastases, and selected for further characterization. Our study revealed that Prdx4 (PrxIV, AOE372) shows functional similarities to other Prx family members by negatively effecting apoptosis induction in tumor cells. In addition, our studies link Prdx4 with Hif-1α, a key regulatory factor of angiogenesis. Targeting Prdx4 may be an attractive approach in cancer therapy, as its inhibition is expected to lead to induction of apoptosis and blockade of Hif-1α-mediated tumor angiogenesis.

2011-06-01 | GSE26571 | GEO

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