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RNA-seq of K562 cells treated with the FTO inhibitor FB23-2

ABSTRACT: RNA-seq of K562 cells treated with the FTO inhibitor FB23-2

PROVIDER: PRJEB52885 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR9735860_1.fastq.gz	Fastqsanger.gz
	ERR9735860_2.fastq.gz	Fastqsanger.gz
	ERR9735855_1.fastq.gz	Fastqsanger.gz
	ERR9735855_2.fastq.gz	Fastqsanger.gz
	ERR9735856_1.fastq.gz	Fastqsanger.gz

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RNA-seq of K562 cells treated with the FTO inhibitor CS2 compared to DMSO treated cells

Project description:Increased FTO expression has been connected to resistance to tyrosine kinase inhibitors in CML. To explore the therapeutic potential of targeting FTO in CML, we tested the FTO catalytic inhibitor in the K562 CML cell line. The RNA-seq was performed to identify relevant regulated genes.

2023-12-31 | E-MTAB-12774 | biostudies-arrayexpress

RNA-seq of K562 cells treated with the FTO inhibitor CS2 compared to DMSO treated cells

Project description:RNA-seq of K562 cells treated with the FTO inhibitor CS2 compared to DMSO treated cells

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RNA-seq of K562 cells treated with the FTO inhibitor FB23-2

Project description:FB23-2 inhibits proliferation of K562 cells. The RNA-seq was performed to identify relevant regulated genes.

2023-12-01 | E-MTAB-11751 | biostudies-arrayexpress

K562-U2AF1_S34F treated with U2AF1-UHM inhibitor, SF1-8

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Sequencing of mRNA with N6-methyladenosine (m6A) modification in AML cells upon DMSO or FTO inhibitor treatment

Project description:To identify the potential mRNA targets of FTO inhibitor, we conducted m6A-seq with mRNA samples enriched from AML cells upon DMSO and FB23-2 (FTO inhibitor) treatment

2019-04-29 | GSE103496 | GEO

HSP90 inhibitor resistant cells

Project description:K562 cells were treated with different HSP90 inhibitors (PuH71 and Coumermycin A1) and the CNV profil was compared to the parental K562 (untreated). In addition, the CNV profile of HSP90AB1 knockout K562 cells was analyzed.

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CNV profile in HSP90 inhibitor resistant K562 cells

Project description:Analysis of the acquired copy number profile in K562 cell which got resistant against HSP90 inhibitors.

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Expression data from Ribonuclease Inhibitor (RI/Rnh1) deficient Human K562 cells

Project description:Summary: Ribonuclease Inhibitor (RI also known as Rnh1) is a 50 kDa, ubiquitously expressed leucine-rich repeat (LRR) protein. It is localized in cytosol and binds to pancreatic-type ribonucleases and inhibit their function. However, the entire biological role for Rnh1 is unknown. We generated RNH1 knock out K562 cells by CRISPR/Cas9 method. Here we studied differential gene expression from wild type and RNH1 knock out K562 cells by RNA-Seq analysis. Overall design: Total RNA was isolated from wild type and RNH1 deficient K562 cells.

2017-03-05 | E-MTAB-5162 | biostudies-arrayexpress

shRNA RNA-seq from K562 (ENCSR688GVV)

Project description:RNA-seq on K562 cells treated with an shRNA knockdown against FTO. (FTO_BGKLV36) For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf

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m6A alterations through FTO in breast cancer [RNA-seq]

Project description:Our understanding of posttranscriptional modifications that decorate RNA, a regulatory layer positioned between DNA and proteins, is in its infancy. N6-methyladenosine (m6A) is the most prevalent internal modification in messenger RNAs that is installed and erased by m6A methyltransferases and demethylases. The importance of these enzymes in cancer is rapidly emerging, yet information of their specific mode of actions during disease progression remain largely unknown. In the present study, we report that the m6A RNA demethylase FTO controls EMT and invasion in cancer through regulation of the Wnt pathway. We find that loss of FTO, in contrast to acute myeloid leukemia, is frequent in many cancer types, including breast and prostate cancers. Knockdown of FTO promotes tumor progression – specifically migration and invasion – in breast and prostate cancer cells. Furthermore, implantation of these cells accelerates tumor progression in recipient mice in vivo. In these tumors, FTO depletion leads to m6A-dependent activation of Wnt signaling, which drives an enhanced EMT program and invasion, thus leading to poor clinical outcome. However, loss of FTO also sensitizes cancers cells to Wnt inhibition, offering a rationale for the therapeutic targeting of Wnt for cancer patients with low FTO levels. Together, our work reveals FTO as a novel regulator of EMT and an unexpected mechanism by which Wnt signals are dysregulated in tumors, providing a rationale to stratify cancer patients treated with Wnt inhibitor. These data uncover a previously unrecognized relationship between RNA modification and EMT in cancer.

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