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Barcode Sequencing Data of Capecitabine Resistant Caco-2 and Irinotecan Resistant HT-29 Cell Lines

ABSTRACT: Barcode Sequencing Data of Capecitabine Resistant Caco-2 and Irinotecan Resistant HT-29 Cell Lines

PROVIDER: PRJEB61117 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR11186650_1.fastq.gz	Fastqsanger.gz
	ERR11186650_2.fastq.gz	Fastqsanger.gz
	ERR11186651_1.fastq.gz	Fastqsanger.gz
	ERR11186651_2.fastq.gz	Fastqsanger.gz
	ERR11186652_1.fastq.gz	Fastqsanger.gz

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Barcode Sequencing Data of Capecitabine Resistant Caco-2 and Irinotecan Resistant HT-29 Cell Lines

Project description:Caco-2 and HT-29 cells were barcoded using the CloneTracker lentiviral barcode library and then irinotecan and capecitabine resistant derivatives of these cell lines were established. Four million barcoded Caco-2 and HT-29 cell were seeded into 15 cm cell culture dishes. When the cells reached confluency, two million cells per dish were seeded into four different 15 cm dishes with 25 mL medium (DMSO Control, Replica A, B, C) and two million cell pellets were stocked as initial cell population.For Caco-2 cell line, mediums in the dishes were changed twice a week with fresh mediums containing IC50 dose (4 months) and subsequently 2x IC50 dose (2 months) of capecitabine, for HT-29 cell line IC50 dose (6 months) of irinotecan. Caco-2 and HT-29 cell lines treated with DMSO were given the same amount of DMSO used in dissolving compounds as fresh medium. Following the end points of six months for each cell line, DNA isolation from harvested cell lines and collected medium of resistant B cell lines were carried out and barcodes were sequenced.

2023-07-11 | E-MTAB-12818 | biostudies-arrayexpress

Barcode and Whole Exome Sequencing Data of Dabrafenib Resistant 3D-HT-29 and Irinotecan Resistant 3D-HCT-116 Spheroids

Project description:HT-29 and HCT-116 cells were barcoded using the CloneTracker lentiviral barcode library and then dabrafenib and irinotecan resistant derivatives of these cell lines were established, respectively.10 million barcoded HT-29 and HCT-116 cells were seeded equally onto poly-HEMA coated 4xT75 flask (DMSO Control, Replica A, B, C for each drug). After seeding, cells were allowed to form spheroids and barcoded 3D-HT-29 spheroids were treated with dabrafenib at increasing doses starting from IC50/10 dose until IC50/2 dose with monthly doubling of the dosing (16 weeks), and barcoded 3D-HCT-116 cells were treated with irinotecan at increasing doses starting from IC50/4 dose until IC50 dose with weekly doubling of the dosing (4 weeks). Following the end points of treatment for each cell line, DNA was isolated from harvested cell lines and barcode sequencing and whole exome sequencing were carried out.

2023-09-01 | E-MTAB-13216 | biostudies-arrayexpress

Expression data from Irinotecan resistant LoVo cells comapred to parental LoVo cells

2014-07-18 | GSE59501 | GEO

Expression data from Irinotecan resistant LoVo cells comapred to parental LoVo cells

Project description:Irinotecan, an analogue of camptothecin, is frequently used in combination with various anticancer drugs or as a single agent in treatment of colorectal cancer. But drug resistance of tumor is still a major obstacle to overcome for the success of cancer treatment. In this study, We established chronic irinotecan resistant cell line for new marker to increase the sensitivity to irinotecan and investigated gene expression profiles of the irinotecan-resistant colorectal cancer cell line. To create stable CRC cell line chronically resistant to Irinotecan, LoVo cell was exposed to an initial Irinotecan concentration of 0.1 M-NM-<mol/L in RPMI 1640 supplemented with 10% FBS. When the growth of the cultured cells reaches at 80% confluency, cells were passaged twice at same drug concentration to ensure adaptation and then concentration of Irinotecan was sequentially increased in the same manner to 8 M-NM-<mol/L and then we investigated the gene expressions between parental colorectal cancer cell line, LoVo and Irinotecan resistant LoVo cell lines

2014-07-18 | E-GEOD-59501 | biostudies-arrayexpress

Barcode and Whole Exome Sequencing Data of Dabrafenib Resistant 3D-HT-29 and Irinotecan Resistant 3D-HCT-116 Spheroids

Project description:Barcode and Whole Exome Sequencing Data of Dabrafenib Resistant 3D-HT-29 and Irinotecan Resistant 3D-HCT-116 Spheroids

| PRJEB64796 | ENA

Expression array of RKO colorectal cancer cells resistant to irinotecan (CPT-11)

Project description:RKO cells and irinotecan resistant derivatives (316 and 526) were compared for expression profile.

2017-06-17 | E-MTAB-5184 | biostudies-arrayexpress

Transcription profiling of topoisomerase I inhibitor irinotecan (CPT-11) sensitive, resistant, and reverted human neuroblastomas

Project description:We have established a neuroblastoma model resistant in vivo to the topoisomerase I inhibitor irinotecan (CPT-11, Camptothecin-11, CAMPTOSAR®) in order to study resistance to these agents acquired in a therapeutic setting. Common mechanisms of resistance were not involved in this model and we thus explored the gene expression signature associated with resistance by comparing the transcriptomes of sensitive, resistant, and reverted tumours using high-throughput DNA microarrays.

2008-01-26 | E-TABM-211 | biostudies-arrayexpress

Barcode Sequencing Data of Dabrafenib Resistant HT-29 Cell Line

Project description:HT-29 cells were barcoded using the CloneTracker lentiviral barcode library and then dabrafenib resistant derivative of these cells were established. Five million barcoded HT-29 cells were seeded into 15 cm cell culture dishes. When the cells reached confluency, two million cells per dish were seeded into four different 15 cm dishes (DMSO Control, Replica A, B, C) and two million cell pellets were stocked as initial cell population. Harvesting used medium through the experiment was performed at monthly intervals. Barcoded HT-29 cell line replicates A, B, and C were treated with 2XIC50 (199.6 nM) of dabrafenib concentration for the duration of 3 months. Following the end points of 3 months for each cell line, DNA isolation from harvested cell lines and collected medium of resistant A cell lines were carried out and barcodes were sequenced.

2023-09-06 | E-MTAB-13018 | biostudies-arrayexpress

Curcumin reverses irinotecan-acquired resistance in colorectal cancer cells: insights from whole transcriptomic data

Project description:To investigate the key mechanisms underlying the acquisition of irinotecan resistance in colorectal cancer cells and the reversal of this resistance by curcumin, we utilized whole-genome microarray expression profiling as a discovery tool to identify the signaling networks involved. Resistance acquisition led to dysregulation of genes associated with irinotecan resistance, including TOP1, drug-metabolizing enzymes (CYPs and UGTs), and efflux transporters (ABCs), while also affecting the extression of 53 genes involed in proliferation and 33 in cell motility. Curcumin treatment significantly modulated 3,901 genes (FC >|±2|), inducing apoptosis, reducing proliferation, and inhibiting migration. Curcumin also enhanced sensitivity to irinotecan, by upregulating TOP1 and inhibiting 18 CYPs, 4 UGTs, and 20 ABCs, including those upregulated in irinotecan-resistant cells.

2025-02-03 | GSE288308 | GEO

Combination effects of capecitabine, irinotecan and 17-AAG on colorectal cancer cell line (HT-29).

Project description:ObjevtiveEvasion of apoptosis is a major feature of cancer cells, therefore designing treatment strategies to target apoptotic pathways seems effective. In this study, we investigate the effect of 17-AAG (17-allylaminogeldanamycin) alone and in double and triple combination with capecitabine (Cap) and irinotecan (IR) on HT-29 colon cancer cell line apoptosis.MethodsCapase-3, 8, 9, p53 and NF-κB genes expression were analyzed by Real-time PCR. DNA laddering assay was performed to confirm Real-time PCR results.ResultsOur results showed that all single treatment groups elevated expression of caspase-3, 8, and 9 significantly and IR/Cap was the only double combination group that could upregulate caspase-8 and -9. NF-κB was down-regulated in single treatment and IR/Cap double combination group, significantly. 17-AAG mono-treatment and IR/Cap and Cap/17-AAG double combination group significantly upregulated p53 gene expression.ConclusionOur findings showed proapoptotic effects of 17-AAG alone and in combination with Cap and IR. These findings propose 17-AAG in combination with routine chemotherapy, as a new protocol for colorectal cancer combination therapy.

| S-EPMC9207062 | biostudies-literature

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