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RNA-Seq of ALDH positive, ALDH negative and unsorted cells from patient-derived 3D in-vitro models of colon cancer

ABSTRACT: RNA-Seq of ALDH positive, ALDH negative and unsorted cells from patient-derived 3D in-vitro models of colon cancer

PROVIDER: PRJEB20298 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1912920_1.fastq.gz	Fastqsanger.gz
	ERR1912920_2.fastq.gz	Fastqsanger.gz
	ERR1912930_1.fastq.gz	Fastqsanger.gz
	ERR1912930_2.fastq.gz	Fastqsanger.gz
	ERR1912940_1.fastq.gz	Fastqsanger.gz

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RNA-Seq of ALDH positive, ALDH negative and unsorted cells from patient-derived 3D in-vitro models of colon cancer

Project description:Fluorescence-activated cell sorting (FACS) was used to separate colon tumor samples into two fractions of ALDH Negative and ALDH Positive cells using the Aldefluor Assay. RNA samples were derived from FAC-sorted 3D in-vitro models of patient-derived colon tumors. Samples from unfractionated in vitro models are also included.

2017-04-30 | E-MTAB-5209 | biostudies-arrayexpress

RNA-Seq of ALDH positive and ALDH negative cells from patient-derived xenograft models of colon cancer

Project description:Colon cancer patient-derived xenograft (PDX) models were processed to single cells and sorted by FACS (BD FACS Aria II) for ALDH activity (Aldefluor assay) and DAPI. ALDH Negative and ALDH Positive cells from each PDX model were collected and lysed in RLT buffer and processed for RNA using the RNeasy Mini Plus RNA extraction kit (Qiagen). Samples were processed using Illumina’s TrueSeq RNA protocol and sequenced on an Illumina HiSeq 2500 machine as 2x125nt paired-end reads. Reads were mapped to the human reference genome (assembly hg19) using the STAR aligner (version 2.4.2a). Total read counts per gene were computed using the program “featureCounts” (version 1.4.6-p2) in the “subread” package, with the gene annotation taken from Gencode (version 19).

2021-01-11 | E-MTAB-8927 | biostudies-arrayexpress

RNA-Seq of ALDH positive and ALDH negative cells from patient-derived xenograft models of colon cancer

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Project description:We used an Aldefluor assay system to study the signaling pathways that regulate the frequency and maintenance of ALDH-positive cell population in MCF-7 cells as a CSC model. Through microarray analysis, we investigated a possible receptor that increases the proportion of the ALDH-positive cell population in MCF-7 cells. MCF-7 were stained with Aldefluor and ALDH-positive cells were sorted using flow cytometry. Gene expression profiles of ALDH+ cells were compared with ALDH- cells.

2014-09-23 | E-GEOD-59653 | biostudies-arrayexpress

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Expression data from ALDH− and ALDH+ shXIst0SUM159 cells treated with or without DOX

Project description:We used microarrays to identify differentially expressed miRNAs in ALDH− and ALDH+ cells treated with or without DOX

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Human colorectal cancer cell line CRC#21: ALDH-high cells vs. ALDH-low cells

Project description:Transcriptional profiling of cancer stem cells (ALDH-high cells) comparing non-cancer stem cells (ALDH-low cells), sorted out using ALDEFLUOR assay. Goal was to identity cancer stem cell-specific genes. Two-condition experiment, sphere-cultured cells vs. adherent-cultured cells: 1 ALDH-high replicate and 1 ALDH-low replicate.

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RNASeq analysis of human ALDH- and ALDH+ DU145 xenografts in nu/nu mice upon radiotherapy treatment

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Project description:Failure to achieve complete elimination of triple negative breast cancer (TNBC) stem cells after adjuvant therapy is associated with poor outcomes. Aldehyde dehydrogenase 1 (ALDH1) is a marker of breast cancer stem cells (BCSCs), and its enzymatic activity regulates tumor stemness. Identifying upstream targets to control ALDH+ cells may facilitate TNBC tumor suppression. Here, we show that KK-LC-1 determines the stemness of TNBC ALDH+ cells via binding with FAT1 and subsequently promoting its ubiquitination and degradation. This compromised the Hippo pathway and led to nuclear translocation of YAP1 and ALDH1A1 transcription. These findings identified the KK-LC-1-FAT1-Hippo-ALDH1A1 pathway in TNBC ALDH+ cells as a therapeutic target. To reverse the malignancy due to KK-LC-1 expression, we employed a novel computational approach and discovered Z839878730 (Z8) as an small-molecule inhibitor which may disrupt KK-LC-1 and FAT1 binding. We demonstrate that Z8 suppressed TNBC tumor growth via a mechanism that reactivated the Hippo pathway and decreased TNBC ALDH+ cell stemness and viability.

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