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BCAT1 regulates glioblastoma cell plasticity and contributes to immunosuppression

ABSTRACT: BCAT1 regulates glioblastoma cell plasticity and contributes to immunosuppression

PROVIDER: PRJNA1037078 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26726136_1.fastq.gz	Fastqsanger.gz
	SRR26726136_2.fastq.gz	Fastqsanger.gz
	SRR26726137_1.fastq.gz	Fastqsanger.gz
	SRR26726137_2.fastq.gz	Fastqsanger.gz
	SRR26726138_1.fastq.gz	Fastqsanger.gz

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BCAT1 regulates glioblastoma cell plasticity and contributes to immunosuppression

Project description:Glioblastoma is the most common malignant brain tumor in adults. Cellular plasticity and the poorly differentiated features result in a fast relapse of the tumors following treatment. Moreover, the immunosuppressive microenvironment proved to be a major obstacle to immunotherapeutic approaches. Branched-chain amino acid transaminase 1 (BCAT1) is a metabolic enzyme that converts branched-chain amino acids into branched-chain keto acids, depleting cellular α-ketoglutarate and producing glutamate. BCAT1 was shown to drive the growth of glioblastoma and other cancers; however, its oncogenic mechanism remains poorly understood. Here, we show that BCAT1 is crucial for maintaining the poorly differentiated state of glioblastoma cells and that its low expression correlates with a more differentiated glioblastoma phenotype. Furthermore, orthotopic tumor injection into immunocompetent mice demonstrated that the brain microenvironment is sufficient to induce differentiation of Bcat1-KO tumors in vivo. We link the transition to a differentiated cell state to the increased activity of TET demethylases and the hypomethylation and activation of neuronal differentiation genes. In addition, the knockout of Bcat1 attenuated immunosuppression, allowing for an extensive infiltration of CD8 + cytotoxic T-cells and complete abrogation of tumor growth. Further analysis in immunodeficient mice revealed that both tumor cell differentiation and immunomodulation following BCAT1-KO contribute to the long-term suppression of tumor growth. In summary, our study unveils BCAT1's pivotal role in promoting glioblastoma growth by inhibiting tumor cell differentiation and sustaining an immunosuppressive milieu. These findings offer a novel therapeutic avenue for targeting glioblastoma through the inhibition of BCAT1.

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Mouse methylation array of glioblastoma mGB2 cells

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BCAT1 contributes to the developmentproliferation and leukemogenesis of TKI-resistant CML

Project description:In this report, we revealed that branched chain amino acid transaminase 1 (BCAT1) is highly enriched in both mouse and human TKI-resistant CML cells. Leukemia was almost completely abrogated upon BCAT1 knockdown during transplantation in a BCR-ABLT315I-induced murine TKI-resistant CML model . Moreover, knockdown of BCAT1 led to a dramatic decrease in the proliferation of TKI-resistant human leukemia cell lines. BCAA/BCAT1 signaling enhanced the phosphorylation of CREB, which is required for maintenance of TKI-resistant CML cells. Importantly, blockade of BCAA/BCAT1 signaling efficiently inhibited leukemogenesis both in vivo and in vitro.

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BCAT1 contributes to the developmentproliferation and leukemogenesis of TKI-resistant CML

Project description:BCAT1 contributes to the developmentproliferation and leukemogenesis of TKI-resistant CML

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RNF20 contributes to epigenetic immunosuppression through CDK9-dependent LSD1 stablization

Project description:RNF20 contributes to epigenetic immunosuppression through CDK9-dependent LSD1 stablization

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BCAT1 expression associates with ovarian cancer progression

Project description:Previously, we have identified cytosolic form of the branched chain amino-acid transaminase 1 (BCAT1) as notably hypomethylated in low-malignant potential (LMP) and high-grade (HG) serous epithelial ovarian tumors, compared to normal ovarian tissues. Here we show that BCAT1 is strongly overexpressed in both LMP and HG serous EOC tumors, thus suggesting that epigenetic mechanisms might be implicated in BCAT1 overexpression in serous epithelial ovarian cancer (EOC). Knockdown of the BCAT1 expression in EOC cells led to sharp decrease of cell proliferation and induced S-phase cell cycle arrest. Additionally, BCAT1 suppression significantly inhibited EOC cell migration and invasion. Gene expression profiling and consecutive network and pathway analyses confirmed these findings, as numerous genes and pathways known previously to be implicated in ovarian tumorigenesis, including EOC tumor invasion and metastasis, were found to be downregulated upon BCAT1 suppression, while some tumor suppressor genes were induced. Taken together, our data are indicative for a strong oncogenic potential of the BCAT1 gene in advanced EOC and identify this transaminase as a novel EOC biomarker and putative EOC therapeutic target.

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Molecular mechanisms of BCAT1 in ASK120067-resistant NSCLC cells

Project description:To investigate the mechanism of BCAT1 in mediating resistance to third-generation EGFR-TKI, we employed RNA-seq analysis to compare the transcriptome signature of ASK120067-resistant NSCLC cells with or without BCAT1 knockdown. Here, gene set enrichment (GSEA) revealed a significant decrease in the expression of genes in glycolysis pathway following small interfering RNA (siRNA)-mediated BCAT1 knockdown, which indicated the role for BCAT1 in supporting TKI resistance through upregulation of glycolysis.

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RNF20 contributes to epigenetic immunosuppression through CDK9-dependent LSD1 stablization (RNA-Seq)

Project description:RNF20 contributes to epigenetic immunosuppression through CDK9-dependent LSD1 stablization (RNA-Seq)

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