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HCT-8 human colorectal cancer (CRC) wild type cells (HCT8/WT) and its 5-FU-induced resistant cell line (HCT8/5-FU)

ABSTRACT: HCT-8 human colorectal cancer (CRC) wild type cells (HCT8/WT) and its 5-FU-induced resistant cell line (HCT8/5-FU)

PROVIDER: PRJNA320265 | ENA |

REPOSITORIES: ENA

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Methylation data from from HCT-8 human colorectal cancer (CRC) wild type cells (HCT8/WT) and its 5-FU-induced resistant cell line (HCT8/5-FU)

Project description:Complete growth medium RPMI-1640 which contains 10% FCS, 1% Penicillin-Streptomycin Solution was used for cell culture. Both cell lines were maintained at 37 °C in a humidified atmosphere containing 5% CO2. MTT assay was performed to determine the 5 ‑ FU resistance in both of HCT-8/WT and HCT-8/5-FU cell line.

2017-03-15 | GSE81006 | GEO

Global expression data from HCT-8 human colorectal cancer (CRC) wild type cells (HCT8/WT) and its 5-FU-induced resistant cell line (HCT8/5-FU)

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Expression profiles of piRNAs in Colorectal Cancer (CRC) cell lines

Project description:To investigate the presence and abundance of piRNAs in Colorectal Cancer (CRC), we performed deep-sequencing of the small RNA transcriptome of eight human CRC cell lines (HT-115, Caco-2, SW-1417, SW 403, COLO 205, HT-29, HCT 116 and RKO).

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YTHDF3 improves translation initiation of mRNAs with N6-methyladenosine methylation at 5’ untranslated region by facilitating eIF2AK2 recruitment in oxaliplatin-resistant colorectal cancer - RNA-seq cell line comparison

Project description:Oxaliplatin as a first-line drug frequently causes the chemo-resistance on colorectal cancer (CRC). N6-methyladenosine (m6A) methylation has been largely acknowledged in multiple biological functions. However, the molecular mechanisms underlying the m6A methylation in modulating anticancer drug resistance in CRC are still obscure. In present study, RNA-seq was conducted to investigate the transcriptome of HCT116, HCT116 cells with oxaliplatin resistance (HCT116R), HCT8 and HCT8 cells with oxaliplatin resistance (HCT8R).

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RNA-seq profiles between human parental and 5-FU drug resistant HCT116 and SW480 colorectal cancer cell lines

Project description:Colorectal cancer (CRC) is one of the most frequently diagnosed and lethal malignancy. Several key factors including poor dietary habits, smoking, alcohol consumption, genetic predisposition, obesity, diabetes mellitus, and sedentary lifestyle – all result in a significantly increased risk for developing CRC. Current treatment modalities for patients with CRC include surgery, which is often followed with adjuvant chemotherapy, especially in patients with a stage II and III disease. Most patients with advanced CRC are generally treated with the chemotherapeutic drug, 5-fluorouracil (5-FU) – either given alone or in combination with oxaliplatin and other molecularly-targeted drugs. While such treatment regimens are effective at improving disease outcomes, their clinical usefulness is often hampered due to the considerable toxicity associated with these treatments, which often causes severe nausea, vomiting, weight loss, and risk of infectious complications due to immunosuppression. Furthermore, their therapeutic efficacy is limited due to the emergence of chemotherapeutic drug resistance. In this study we performed genomewide transcriptomic analysis of parental and 5-FU resistant cells to identify differentially expressed genes and its associated pathways in promoting chemoresistance in CRC.

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RNAseq analysis of DDX21-silenced colorectal cancer cell HCT8

Project description:DEAD-box RNA helicase 21 (DDX21), is a nucleolar protein harboring ATP-dependent double-stranded RNA unwinding activities, essential in rRNA processing and ribosome biogenesis. However, its role in colorectal cancer (CRC) progression remains unclear. In this study, we performed RNAseq in colorectal cancer line HCT8 with or without DDX21 gene silencing, to reveal the role of DDX21 in transcriptional and epigenetic control of CRC cell proliferation.

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Downregulation of KRAB zinc finger proteins in 5-fluorouracil resistant colorectal cancer cells

Project description:The radio-chemotherapy with 5-fluorouracil (5-FU) is the standard of care treatment for patients with locally advanced rectal cancer (LARC) but it is only effective for a third of them. The proteomic and transcriptomic response of three colorectal cancer (CRC) cell lines to 5-FU and radiation was assessed and correlated with their genetic background. The induction of a 5-FU-resistance in those cell lines negatively affects the levels of transcripts corresponding to Krüppel-associated box (KRAB)-containing zinc finger proteins (ZFPs), the largest family of transcriptional repressors. Among nearly 350 KRAB-ZFPs, almost a quarter are down-regulated after the induction of a 5-FU-resistance including a common one between the three CRC cell lines, ZNF649, whose role is still unknown. This proteomic, transcriptomic and genomic analysis of intrinsic and acquired resistance highlights possible new mechanisms involved in resistance to treatment and therefore potential new therapeutic targets to overcome this resistance.

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Project description:In the present study, we investigated miRNA expression changes caused by aquired chemoresistance to 5-FU or Oxa. 40 and 14 miRNAs were detected as differentially expressed in 5-fluouracil- and oxaliplatin-resistant colorectal HCT116 sublines, respectively. Differentially expressed miRNAs determined in the present study could be applied for further development of diagnostic and therapeutic applications for colorectal cancer carcinoma resistant to 5-FU or Oxa.

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Homo sapiens

Project description:Methylation data from from HCT-8 human colorectal cancer (CRC) wild type cells (HCT8/WT) and its 5-FU-induced resistant cell line (HCT8/5-FU)

| PRJNA320267 | ENA

Homo sapiens

Project description:Global expression data from HCT-8 human colorectal cancer (CRC) wild type cells (HCT8/WT) and its 5-FU-induced resistant cell line (HCT8/5-FU)

| PRJNA320268 | ENA

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