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

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

PROVIDER: PRJNA889443 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21864450_1.fastq.gz	Fastqsanger.gz
	SRR21864450_2.fastq.gz	Fastqsanger.gz
	SRR21864451_1.fastq.gz	Fastqsanger.gz
	SRR21864451_2.fastq.gz	Fastqsanger.gz
	SRR21864452_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 [CRISPR screen]

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

| PRJNA891260 | ENA

A CRISPR-Cas9 library screening identifies CARM1 as a critical inhibitor of ferroptosis in hepatocellular carcinoma cells

Project description: Not available

| S-EPMC10661451 | biostudies-literature

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

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

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

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

Genome-wide CRISPR/Cas9 library screening identified PHGDH as a critical driver for Sorafenib resistance in HCC.

Project description:Sorafenib is the standard treatment for advanced hepatocellular carcinoma (HCC). However, the development of drug resistance is common. By using genome-wide CRISPR/Cas9 library screening, we identify phosphoglycerate dehydrogenase (PHGDH), the first committed enzyme in the serine synthesis pathway (SSP), as a critical driver for Sorafenib resistance. Sorafenib treatment activates SSP by inducing PHGDH expression. With RNAi knockdown and CRISPR/Cas9 knockout models, we show that inactivation of PHGDH paralyzes the SSP and reduce the production of αKG, serine, and NADPH. Concomitantly, inactivation of PHGDH elevates ROS level and induces HCC apoptosis upon Sorafenib treatment. More strikingly, treatment of PHGDH inhibitor NCT-503 works synergistically with Sorafenib to abolish HCC growth in vivo. Similar findings are also obtained in other FDA-approved tyrosine kinase inhibitors (TKIs), including Regorafenib or Lenvatinib. In summary, our results demonstrate that targeting PHGDH is an effective approach to overcome TKI drug resistance in HCC.

| S-EPMC6794322 | biostudies-literature

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