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CRISPR/Cas9 screens reveal that hexokinase 2 enhances cancer stemness and tumorigenicity

ABSTRACT: CRISPR/Cas9 screens reveal that hexokinase 2 enhances cancer stemness and tumorigenicity

PROVIDER: PRJNA766529 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16081332_1.fastq.gz	Fastqsanger.gz
	SRR16081332_2.fastq.gz	Fastqsanger.gz
	SRR16081333_1.fastq.gz	Fastqsanger.gz
	SRR16081333_2.fastq.gz	Fastqsanger.gz
	SRR16081334_1.fastq.gz	Fastqsanger.gz

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CRISPR/Cas9 screens reveal that hexokinase 2 enhances cancer stemness and tumorigenicity

Project description:We identified that HK2 facilitate the maintenance and self-renewal of liver cancer stem cells (CSCs). Moreover, HK2 exerts its function by enhancing the accumulation of acetyl-CoA and epigenetically activating the transcription of acyl-CoA synthetase long chain family member 4 (ACSL4), leading to an increase in fatty acid β-oxidation (FAO) activity.

2022-05-06 | GSE184798 | GEO

CRISPR/Cas9 Screens Reveal that Hexokinase 2 Enhances Cancer Stemness and Tumorigenicity by Activating the ACSL4-Fatty Acid β-Oxidation Pathway.

Project description:Metabolic reprogramming is often observed in carcinogenesis, but little is known about the aberrant metabolic genes involved in the tumorigenicity and maintenance of stemness in cancer cells. Sixty-seven oncogenic metabolism-related genes in liver cancer by in vivo CRISPR/Cas9 screening are identified. Among them, acetyl-CoA carboxylase 1 (ACC1), aldolase fructose-bisphosphate A (ALDOA), fatty acid binding protein 5 (FABP5), and hexokinase 2 (HK2) are strongly associated with stem cell properties. HK2 further facilitates the maintenance and self-renewal of liver cancer stem cells. Moreover, HK2 enhances the accumulation of acetyl-CoA and epigenetically activates the transcription of acyl-CoA synthetase long-chain family member 4 (ACSL4), leading to an increase in fatty acid β-oxidation activity. Blocking HK2 or ACSL4 effectively inhibits liver cancer growth, and GalNac-siHK2 administration specifically targets the growth of orthotopic tumor xenografts. These results suggest a promising therapeutic strategy for the treatment of liver cancer.

| S-EPMC9313492 | biostudies-literature

Chronic stress dampens Lactobacillus johnsonii-driven suppression on cancer stemness and enhances colorectal tumorigenicity

Project description:Chronic stress dampens Lactobacillus johnsonii-driven suppression on cancer stemness and enhances colorectal tumorigenicity

| PRJNA868205 | ENA

A PRC2-KDM5B-stemness regulatory axis sustains tumorigenicity of acute myeloid leukemia [ChIP-Seq]

Project description:Acute myeloid leukemias (AMLs) with the NUP98-NSD1 or MLL gene rearrangement (MLL-r) share transcriptomic profiles featured with stemness-related gene signatures and display poor prognosis in the clinic. However, the molecular underpinnings of AML aggressiveness and stemness remain far from clear. Here, we report that the enzymatic activity of Polycomb Repressive Complex 2 (PRC2) is crucial for maintenance of tumorigenicity in NUP98-NSD1+ AML, consistent to its role in MLL-r AML. Transcriptomic analysis revealed Kdm5b, a lysine demethylase gene carrying the “bivalent domain” chromatin feature in AML, to be directly repressed by PRC2. While ectopic expression of Kdm5b suppressed AML growth, its depletion in AML not only promoted tumorigenicity but also significantly attenuated anti-AML effects by PRC2 inhibitors, thus demonstrating an involvement of the PRC2-|Kdm5b axis for AML oncogenesis. Lower KDM5B expression is positively correlated with poorer prognosis of human AML patients. RNA-seq, ChIP-seq and CUT&RUN based genomic profilings also showed that Kdm5b directly binds to and represses AML stemness genes. In contrast to an essential involvement for its various chromatin-associating domains, Kdm5b’s demethylase function was found to be dispensable for AML suppression, indicating a scaffold role in assembling gene-repressive complexes. Collectively, this study describes a molecular axis involving histone modifiers (PRC2 and Kdm5b) for sustaining the malignant features of AML, implicative of potential therapeutics.

2022-02-22 | GSE179824 | GEO

A PRC2-KDM5B-stemness regulatory axis sustains tumorigenicity of acute myeloid leukemia [CUT&RUN]

2022-02-22 | GSE179168 | GEO

A PRC2-KDM5B-stemness regulatory axis sustains tumorigenicity of acute myeloid leukemia [RNA-Seq]

2022-02-22 | GSE179167 | GEO

High-fat diet activated fatty acid oxidation mediates intestinal stemness and tumorigenicity

Project description:High-fat diet activated fatty acid oxidation mediates intestinal stemness and tumorigenicity

| PRJNA705719 | ENA

High-fat diet activated fatty acid oxidation mediates intestinal stemness and tumorigenicity

Project description:High-fat diet activated fatty acid oxidation mediates intestinal stemness and tumorigenicity

| PRJNA692179 | ENA

A PRC2-KDM5B-stemness regulatory axis sustains tumorigenicity of acute myeloid leukemia

Project description:A PRC2-KDM5B-stemness regulatory axis sustains tumorigenicity of acute myeloid leukemia

| PRJNA745183 | ENA

CRISPR Cas9 screens for drug resistance in AML cell lines

Project description:Acute myeloid leukaemia (AML) continues to have a very high mortality and its treatment hasnot changed for more than 20 years.Here, we propose to apply genomic-wide screens to directly identify therapeutic vulnerabilitiesof AML using AML cells lines with pre-defined somatic mutations. Our studies will be basedon genome-wide CRISPR/CAs9 gRNA screens and will be used to identify drivers of drugresistance to standard chemotherapies.This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/

2015-02-03 | E-ERAD-335 | biostudies-arrayexpress

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