Ontology highlight
ABSTRACT:
PROVIDER: PRJNA787102 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The aim of this study was to identify chemoresistance-associated genes in hepatocellular carcinoma (HCC). cDNA microarray analysis was performed to compare the mRNA expression profiles of a human metastatic HCC cell line (named MHCC97Low) and its derived chemoresistant sublines including cisplatin resistant subline (named MHCC97L/CisR or C8) and doxorubicin resistant subline (named MHCC97L/DoxR or D5). Total RNAs were extracted from MHCC97Low (97Low as sample name), MHCC97L/CisR (C8 as sample name) and MHCC97L/DoxR (D5 as sample name), and hybridized on Affymetrix microarrays. We planed to identify differential genes between 97Low and C8 (cisplatin resistant genes) as well as to identify differential genes between 97Low and D5 (doxorubicin resistant genes).
2014-01-17 | E-GEOD-54175 | biostudies-arrayexpress
Project description:The aim of this study was to identify chemoresistance-associated genes in hepatocellular carcinoma (HCC). cDNA microarray analysis was performed to compare the mRNA expression profiles of a human metastatic HCC cell line (named MHCC97Low) and its derived chemoresistant sublines including cisplatin resistant subline (named MHCC97L/CisR or C8) and doxorubicin resistant subline (named MHCC97L/DoxR or D5).
2014-01-17 | GSE54175 | GEO
Project description:To identify genes associated with HCC invasiveness and metastasis, a hybridization-based microarray assay was used to analyze three cell lines with increasing metastatic potentials, Huh7,MHCC97L, and HCCLM3
2017-04-12 | GSE97626 | GEO
Project description:The Facilitates Chromatin Transcription (FACT) is involved in chromatin remodeling during transcription, replication and DNA repair and is considered to be an ubiquitously expressed complex that has no known associations with any disease. However, we discovered that FACT is expressed in very limited number of cells of adult mammalian organism, mostly presented by stem and undifferentiated cells. Here, we show that FACT is present in poorly differentiated aggressive cancers with an overall low survival rate. FACT acts as an "accelerator" of tumor transformation. It cannot drive transformation like an oncogene, but it increases the efficiency of oncogene-induced transformation. FACT expressing cancer cells cannot grow in the absence of FACT possibly due to the FACT involvement in selective chromatin remodeling of genes that stimulate proliferation, inhibit cell death and differentiation and that are induced in response to cell stress. We propose that FACT is a marker of an aggressive cancer phenotype and Patients with FACT-positive tumors are noted for an overall poorer survival rate. FACT expression in primary tumors may be used as a predictor of metastatic disease. FACT may also be used as a target of anti-cancer therapy because tumor cells expressing FACT are dependent on FACT function, while normal cells either do not express FACT or are not sensitive to FACT inhibition. Examination of AR binding sites of 3 replicates of untreated cells and 3 replicates of curaxin-treated cells, each with 3 replicate controls
2013-03-22 | E-GEOD-45393 | biostudies-arrayexpress
Project description:Interventions: experimental group :PD-1 Knockout Engineered T Cells
Primary outcome(s): Number of participants with Adverse Events and/or Dose Limiting Toxicities as a Measure of Safety and tolerability of dose of PD-1 Knockout T cells using Common Terminology Criteria for Adverse Events (CTCAE v4.0) in patients
Study Design: historical control
| 2662961 | ecrin-mdr-crc
Project description:Histone chaperone FACT is commonly expressed and essential for the viability of transformed but not normal cells and its expression levels correlate with poor prognosis in cancer patients. FACT binds several components of nucleosomes and has been viewed as a factor destabilizing nucleosomes to facilitate RNA polymerase passage. To connect FACT’s role in transcription with the viability of tumor cells, we analyzed genome-wide FACT binding to chromatin in conjunction with transcription in mouse and human cells with different degrees of FACT dependence. While genomic distribution and density of FACT correlated with the intensity of transcription, FACT knockout or knockdown was unexpectedly accompanied by the elevation, rather than suppression, of transcription and with the destabilization of chromatin. These data suggest that the real function of FACT is to stabilize and reassemble nucleosomes disturbed by transcription. This function is apparently vital for tumor cells because malignant transformation is accompanied by chromatin destabilization.
2019-06-12 | GSE132576 | GEO
Project description:The Facilitates Chromatin Transcription (FACT) is involved in chromatin remodeling during transcription, replication and DNA repair and is considered to be an ubiquitously expressed complex that has no known associations with any disease. However, we discovered that FACT is expressed in very limited number of cells of adult mammalian organism, mostly presented by stem and undifferentiated cells. Here, we show that FACT is present in poorly differentiated aggressive cancers with an overall low survival rate. FACT acts as an "accelerator" of tumor transformation. It cannot drive transformation like an oncogene, but it increases the efficiency of oncogene-induced transformation. FACT expressing cancer cells cannot grow in the absence of FACT possibly due to the FACT involvement in selective chromatin remodeling of genes that stimulate proliferation, inhibit cell death and differentiation and that are induced in response to cell stress. We propose that FACT is a marker of an aggressive cancer phenotype and Patients with FACT-positive tumors are noted for an overall poorer survival rate. FACT expression in primary tumors may be used as a predictor of metastatic disease. FACT may also be used as a target of anti-cancer therapy because tumor cells expressing FACT are dependent on FACT function, while normal cells either do not express FACT or are not sensitive to FACT inhibition.
2013-03-22 | GSE45393 | GEO
Project description:RNAseq measurement of cortisol induced gene expression change under knockout of Klf9
| PRJNA605203 | ENA