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A CRISPR/Cas9 library screening identified CARM1 as a critical inhibitor for Sorafenib-induced ferroptosis in hepatocellular carcinoma cells [CRISPR screen]

ABSTRACT: A CRISPR/Cas9 library screening identified CARM1 as a critical inhibitor for Sorafenib-induced ferroptosis in hepatocellular carcinoma cells [CRISPR screen]

PROVIDER: PRJNA891260 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21931100_1.fastq.gz	Fastqsanger.gz
	SRR21931100_2.fastq.gz	Fastqsanger.gz
	SRR21931096_1.fastq.gz	Fastqsanger.gz
	SRR21931096_2.fastq.gz	Fastqsanger.gz
	SRR21931097_1.fastq.gz	Fastqsanger.gz

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A CRISPR/Cas9 library screening identified CARM1 as a critical inhibitor for Sorafenib-induced ferroptosis in hepatocellular carcinoma cells

Project description:CARM1 inhibits ferroptosis through promoting the transcription of GPX4. HepG2 cells expressing control shRNAs or CARM1 shRNAs were treated with Sorafenib for 24 hours, and then the mRNAs were extracted and subjected to RNA-seq.

2023-01-01 | GSE215263 | GEO

A CRISPR/Cas9 library screening identified CARM1 as a critical inhibitor for Sorafenib-induced ferroptosis in hepatocellular carcinoma cells [CRISPR screen]

Project description:To find epigenetic factors potentially involved in Sorafenib resistance in hepatocellular carcinoma cells, an epigenetic factors-targeted CRISPR/Cas9 library was applied to perform the screening.

2023-01-01 | GSE215909 | GEO

A CRISPR/Cas9 library screening identified CARM1 as a critical inhibitor for Sorafenib-induced ferroptosis in hepatocellular carcinoma cells

Project description:A CRISPR/Cas9 library screening identified CARM1 as a critical inhibitor for Sorafenib-induced ferroptosis in hepatocellular carcinoma cells

| PRJNA889443 | ENA

YAP/TAZ and ATF4 collaboratively drive resistance to Sorafenib therapy in hepatocellular carcinoma by preventing ferroptosis

Project description:Understanding the mechanisms underlying evasive resistance in cancer is an unmet medical need to improve the efficacy of current therapies. In this study, a combination of shRNA-mediated synthetic lethality screening and transcriptomic analysis revealed the transcription factors YAP/TAZ as key drivers of Sorafenib resistance in hepatocellular carcinoma (HCC) by repressing Sorafenib-induced ferroptosis. Mechanistically, in a TEAD-dependent manner YAP/TAZ induce the expression of SLC7A11, a key transporter maintaining intracellular glutathione homeostasis, thus enabling HCC cells to overcome Sorafenib-induced ferroptosis. At the same time, YAP/TAZ sustain the protein stability, nuclear localization and transcriptional activity of ATF4 which in turn cooperates to induce SLC7A11 expression. Our study uncovered a critical role of YAP/TAZ in the repression of ferroptosis and thus in the establishment of Sorafenib resistance in HCC, highlighting YAP/TAZ-based rewiring strategies as potential approaches to overcome HCC therapy resistance.

2021-08-20 | GSE181771 | GEO

Genome wide CRISPR screen for Sorafenib resistance in MOLM13 and MV411 cells using Y. Kosuke library

Project description:MOLM13 or MV411 cells were generated to express Cas9, infected with CRISPR library (Tzelepis et al 2016) , selected for puromycin resistance and exposed to Sorafenib (50nM), Crenolanib (20nM) or vehicle, DMSO. Cells were collected at time 0 (post puromycin selection), day 7 and 14 for Sorafenib as well as 14 and 21 for Crenolanib. DNA was extracted and sgRNA barcodes were amplified. The resulting PCR library was deep sequenced using the Illumina HiSeq 2500 using 6 samples per lane.

2021-05-19 | GSE138343 | GEO

USP22 promotes the proliferation and inhibits Sorafenib-induced ferroptosis of hepatocellular carcinoma cells through its deubiquitinase activity

Project description:Hepatocellular carcinoma (HCC) remains one of the most lethal cancers, characterized by poor prognosis and low life expectancy. Unfortunately, there are very few molecular therapeutic options available for advanced HCC. Sorafenib is a current standard first-line treatment for advanced HCC, but drug resistance significantly limits its therapeutic efficacy. In this study, we identified ubiquitin-specific protease 22 (USP22) as the key regulator of HCC development and Sorafenib resistance. Analysis of TCGA databases revealed that USP22 is highly expressed in HCC tissues and is closely associated with poor patient prognosis. Our data further indicated that USP22 promotes the proliferation of HCC cells via deubiquitinating and stabilizing cyclin-dependent kinase 11B (CDK11B). Additionally, USP22 acts as a novel inducer of Sorafenib resistance and suppresses Sorafenib-triggered ferroptosis in HCC cells. It reduces the transcription of the transferrin receptor (TFRC) by decreasing H2BK120ub occupancy at TFRC transcription start site (TSS) downstream region, thereby inhibiting ferroptosis upon Sorafenib treatment. Finally, animal experiments confirmed the role of USP22 in promoting HCC cell growth and Sorafenib resistance in vivo. Taken together, our findings suggest that USP22 represents a promising prognostic biomarker and therapeutic target for HCC patients, particularly those with Sorafenib resistance.

2024-10-03 | GSE278684 | GEO

RNA seq data of sorafenib resistant HepG2 cells

Project description:To investigate the molecular mechanism of ferroptosis resistance in HCC, we applied sorafenib, one of the class I ferroptosis inducers (FINs), to generate HepG2 sorafenib resistant (SR) cells.

2024-02-03 | GSE248764 | GEO

USP22 promotes the proliferation and inhibits Sorafenib-induced ferroptosis of hepatocellular carcinoma cells through its deubiquitinase activity [ChIP-seq]

2024-10-03 | GSE278685 | GEO

Quantitative Time-Course Profiling of Sorafenib-Treated Hepatocellular Carcinoma (HCC) Cells Through Phosphoproteome Analysis

Project description:Ferroptosis is a new form of regulated, non-apoptotic cell death characterized by excessive lipid peroxidation upon loss of activity of the lipid repair enzyme glutathione peroxidase 4 (GPX4). Sorafenib, an FDA-approved multi-kinase inhibitor drug for treatment of hepatocellular carcinoma (HCC), has been shown to induce ferroptosis. Protein phosphorylation changes upon Sorafenib treatment have been previously reported in patient studies and in cell culture however the early phosphorylation changes during induction of ferroptosis are not completely understood. This work highlights these changes through a time course from 7 to 60 min of Sorafenib treatment in SKHep1 cells to provide insight on the induction of ferroptosis. 6,186 unique phosphosites were quantified from 2,381 phosphoproteins in this study and phosphorylation changes occurred in as early as 30 minutes of Sorafenib treatment. By 60 minutes, significant changes in key regulatory pathways were identified, including sites from ferroptosis-related proteins, indicating the involvement of phospho-regulated signaling during ferroptosis induction.

2019-07-26 | MSV000084140 | MassIVE

CRISPR screens uncover protective effect of PSTK to targeted therapy induced ferroptosis in hepatocellular carcinoma

Project description:Hepatocellular carcinoma (HCC) is one of the most frequent malignancies with extremely poor prognosis. Clinical efficacies of existing targeted therapy strategies were not satisfied due to targeted therapy resistance. In this study, we performed a series of CRISPR/Cas9 screens to identify synthetic lethality genes to improve the clinical response of HCC. CRISPR loss-of-function genetic screens were performed to identify synthetic lethality genes of targeted therapies (Abemaciclib, Palbociclib, Sorafenib, Lenvatinib, Regorafenib and Erastin) in HCC cell lines. RNA-seq analysis were performed to clarify potential mechanism. We identified that inhibition of phosphoseryl-tRNA kinase (PSTK) sensitized HCC cells to targeted therapies. PSTK contributes to resistance of targeted therapy induced ferroptosis.

2022-03-23 | GSE182185 | GEO

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