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ADAR1-mediated RNA editing of SCD1 links lipid metabolism to gastric cancer drug resistance and self-renewal

ABSTRACT: The University of Hong Kong Gastric Cancer Drug Treatment Study

PROVIDER: PRJEB60472 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR10975857_1.fastq.gz	Fastqsanger.gz
	ERR10975857_2.fastq.gz	Fastqsanger.gz
	ERR10975858_1.fastq.gz	Fastqsanger.gz
	ERR10975858_2.fastq.gz	Fastqsanger.gz
	ERR10975859_1.fastq.gz	Fastqsanger.gz

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ADAR1-mediated RNA editing of SCD1 drives drug resistance and self-renewal in gastric cancer.

Project description:Targetable drivers governing 5-fluorouracil and cisplatin (5FU + CDDP) resistance remain elusive due to the paucity of physiologically and therapeutically relevant models. Here, we establish 5FU + CDDP resistant intestinal subtype GC patient-derived organoid lines. JAK/STAT signaling and its downstream, adenosine deaminases acting on RNA 1 (ADAR1), are shown to be concomitantly upregulated in the resistant lines. ADAR1 confers chemoresistance and self-renewal in an RNA editing-dependent manner. WES coupled with RNA-seq identify enrichment of hyper-edited lipid metabolism genes in the resistant lines. Mechanistically, ADAR1-mediated A-to-I editing on 3'UTR of stearoyl-CoA desaturase (SCD1) increases binding of KH domain-containing, RNA-binding, signal transduction-associated 1 (KHDRBS1), thereby augmenting SCD1 mRNA stability. Consequently, SCD1 facilitates lipid droplet formation to alleviate chemotherapy-induced ER stress and enhances self-renewal through increasing β-catenin expression. Pharmacological inhibition of SCD1 abrogates chemoresistance and tumor-initiating cell frequency. Clinically, high proteomic level of ADAR1 and SCD1, or high SCD1 editing/ADAR1 mRNA signature score predicts a worse prognosis. Together, we unveil a potential target to circumvent chemoresistance.

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