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Molecular mechanisms of BCAT1 in ASK120067-resistant NSCLC cells

ABSTRACT: Molecular mechanisms of BCAT1 in ASK120067-resistant NSCLC cells

PROVIDER: PRJNA1039771 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26807794_1.fastq.gz	Fastqsanger.gz
	SRR26807794_2.fastq.gz	Fastqsanger.gz
	SRR26807795_1.fastq.gz	Fastqsanger.gz
	SRR26807795_2.fastq.gz	Fastqsanger.gz
	SRR26807796_1.fastq.gz	Fastqsanger.gz

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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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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 Confers Resistance to EGFR TKIs through α-KG-dependent Epigenetic Regulation of the Glycolysis Pathway in NSCLC

Project description:Epidermal growth factor receptor (EGFR) mutations are leading oncogenic drivers in non-small cell lung cancer (NSCLC). Many third-generation EGFR tyrosine kinase inhibitors (TKIs) have been developed to target EGFR T790M and activating mutations. Osimertinib (AZD9291) was the first approved drug and is now the standard-of-care therapy for untreated EGFR-mutated NSCLC. Our team previously identified ASK120067, for which we have submitted a new drug application (NDA) in China. Although third-generation EGFR TKIs exhibit favorable antitumor effects in NSCLC treatment, acquired resistance with largely unexplored mechanisms still limits their long-term efficacy. In this study, we aimed to investigate the molecular mechanisms underlying resistance to EGFR TKIs and identify new therapeutic strategies for the treatment of NSCLC. Methods: Elevated expression of BCAT1 in EGFR TKI-resistant lung cancer cells was identified using stable isotope labeling by amino acids in cell culture (SILAC)-based proteomics analysis and verified with Western blotting and RT‒qPCR.

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