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CRISPR screens uncover CRTC3 as a regulator of IFN-γ induced ferroptosis in hepato-cellular carcinoma [CRISPR screen]

ABSTRACT: CRISPR screens uncover CRTC3 as a regulator of IFN-γ induced ferroptosis in hepato-cellular carcinoma [CRISPR screen]

PROVIDER: PRJNA852589 | ENA |

REPOSITORIES: ENA

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CRISPR screens uncover CRTC3 as a regulator of IFN-γ induced ferroptosis in hepato-cellular carcinoma

Project description:CRISPR screens uncover CRTC3 as a regulator of IFN-γ induced ferroptosis in hepato-cellular carcinoma

| PRJNA852587 | ENA

CRISPR screens uncover CRTC3 as a regulator of IFN-γ induced ferroptosis in hepato-cellular carcinoma [CRISPR screen]

Project description:Gamma interferon (IFN-γ) was reported to exhibit anti-tumor effects via inducing ferroptosis. Based on genome-wide CRISPR/Cas9 knockout screens, we discovered that cAMP response ele-ment binding protein (CREB) regulated transcription coactivator3 (CRTC3) protects tumor cells from drug induced ferroptosiis and is a significant resister of IFN-γ treatment in hepatocellular car-cinoma (HCC). Mechanically, CRTC3 knockout alters tumor cell lipid pattern and increases the abundance of polyunsaturated fatty acids (PUFAs), which facilitates lipid peroxidation and renders HCC cells susceptible to ferroptosis inducers. To scavenge accumulated lipid peroxides (LPO) and maintain redox equilibrium, HCC cells upregulate SLC7A11 expression to enhance the activity of glutamate-cystine antiporter (system xc-). As IFN-γ inhibiting system xc-, simultaneously treatment of IFN-γ disrupts the compensatory mechanism, and generates a synergistic effect with CRTC3 knockout to facilitate ferroptosis. The sensitizing effect of CRTC3 depletion was further confirmed in typical ferroptosis inducers including RSL3, Erastin and Sorafeinib. Here, we reported a hitherto unexpected role of CRTC3 in regulating PUFAs metabolism and ferroptosis. Targeting the CRTC3 signaling in combination with ferroptosis inducers may represent a viable approach to treat cancer and overcome drug resistance in HCC.

2025-06-24 | GSE206905 | GEO

CRISPR screens uncover CRTC3 as a regulator of IFN-γ induced ferroptosis in hepato-cellular carcinoma [RNA-seq]

2025-06-24 | GSE206906 | GEO

CRISPR screens uncover CRTC3 as a regulator of IFN-γ induced ferroptosis in hepato-cellular carcinoma [RNA-seq]

Project description:CRISPR screens uncover CRTC3 as a regulator of IFN-γ induced ferroptosis in hepato-cellular carcinoma [RNA-seq]

| PRJNA852588 | ENA

CRISPR screens uncover CRTC3 as a regulator of IFN-γ induced ferroptosis in hepato-cellular carcinoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-06-24 | GSE206907 | GEO

Genome-Scale Exon Perturbation Screens Uncover Critical Exons for Cell Fitness [CRISPR]

Project description:Genome-Scale Exon Perturbation Screens Uncover Critical Exons for Cell Fitness [CRISPR]

| PRJNA1022426 | ENA

Pooled CRISPR screens in human intestinal organoids [CRISPR screens]

Project description:Pooled CRISPR screens in human intestinal organoids [CRISPR screens]

| PRJNA608420 | ENA

CRISPR-MIP replaces PCR and reveals GC and oversampling bias in pooled CRISPR screens

Project description:This is data for the evaluation of a new way of counting sgRNAs in CRISPR screens using padlock probes and UMIs. It is compared to the typical PCR-based approach. In particular, a dropout screen was performed in MiaPaCa-2 cells using the Human Kinome CRISPR pooled library (Addgene #75314)

2024-08-18 | E-MTAB-14379 | biostudies-arrayexpress

Transcript profiling in WT, CRTC3 KO and CRTC3-rescued B16F1 cells.

Project description:Triggering of cAMP and mitogen-activated (MAPK) pathways in response to hormonal and growth factor cues promotes melanocyte pigmentation and survival in part through induction of the master regulator MITF by cAMP-responsive factor CREB. We examined the role of CREB coactivators (CRTC1-3) in transduction of cAMP and MAPK signals in melanocytes. We found that CRTC3 knock-out in mice and B16F1 melanoma cells decreases pigmentation by directly regulating the expression of the melanosomal transporter OCA2. In addition to effects of cAMP, CRTC3 activation was also promoted by ERK1/2-mediated phosphorylation at Ser391; amounts of phosphorylated CRTC3-S391 were constitutively elevated in human melanoma cells expressing mutated BRAF or NF1. Knock-out of CRTC3 in A375 melanoma cells impaired their anchorage-independent growth, migration and invasiveness, whereas CRTC3 over-expression increased survival in response to BRAF inhibition by vemurafenib. Analysis of spontaneous CRTC3 mutations in melanomas reveals that increased activity of this co-activator associates with reduced patient survival. Our results highlight the importance of CRTC3 in pigmentation and melanoma progression.

2022-04-12 | GSE154115 | GEO

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

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

| PRJNA755280 | ENA