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ADAT2/3 complex-deposited tRNA inosines drives oncogenic transformation

ABSTRACT: ADAT2/3 complex-deposited tRNA inosines drives oncogenic transformation

PROVIDER: PRJNA980179 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24828555.fastq.gz	Fastqsanger.gz
	SRR24828556.fastq.gz	Fastqsanger.gz
	SRR24828557.fastq.gz	Fastqsanger.gz
	SRR24828558.fastq.gz	Fastqsanger.gz
	SRR24828559.fastq.gz	Fastqsanger.gz

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ADAT2/3 complex-deposited tRNA inosines drives oncogenic transformation

Project description:Transfer RNAs (tRNAs) are subject to numerous posttranscriptional modifications that influence their maturation, stability, and function. Adenosine to Inosine (A-to-I) editingin thetRNA anticodon stem loop is an important modification that influences anticodon-codon recognition.However,the implications of tRNA editing in cancer and its potential for diagnostic and therapeutic applicationsare not yet well understood.We showed that the ADAT2/3 enzyme complex, responsible for this modification in humans, is amplified and overexpressed in several tumor types,with a higher amplification rate in sarcoma tumors, particularly liposarcomas. We determine that the ADAT complex works as an oncogene in these tumors and that its inhibition reduces tumor growth, offering a new approach to cancer treatment. In addition, we provided insight into the mechanisms of cancer development and progression, demonstrating that tRNA editing is required for higher mRNA translation of oncogenic proteins enriched with specific ADAT-sensitive codons. Thus, ADAT-mediated tRNA modification drives oncogenic transformation by remodeling the set of mRNAs being actively translated to increase expression of proteins that promote proliferation. Our results explain how cancer cells benefit from increased tRNA A-to-I editing and propose ADATs as potential therapeutic targets for the treatment of cancer.

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METTL1-mediated m7G tRNA modification drives oncogenic transformation

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METTL1-mediated m7G tRNA modification drives oncogenic transformation

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

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STRIPAK directs PP2A activity to promote oncogenic transformation

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METTL1-mediated m<sup>7</sup>G modification of Arg-TCT tRNA drives oncogenic transformation.

Project description:The emerging "epitranscriptomics" field is providing insights into the biological and pathological roles of different RNA modifications. The RNA methyltransferase METTL1 catalyzes N7-methylguanosine (m7G) modification of tRNAs. Here we find METTL1 is frequently amplified and overexpressed in cancers and is associated with poor patient survival. METTL1 depletion causes decreased abundance of m7G-modified tRNAs and altered cell cycle and inhibits oncogenicity. Conversely, METTL1 overexpression induces oncogenic cell transformation and cancer. Mechanistically, we find increased abundance of m7G-modified tRNAs, in particular Arg-TCT-4-1, and increased translation of mRNAs, including cell cycle regulators that are enriched in the corresponding AGA codon. Accordingly, Arg-TCT expression is elevated in many tumor types and is associated with patient survival, and strikingly, overexpression of this individual tRNA induces oncogenic transformation. Thus, METTL1-mediated tRNA modification drives oncogenic transformation through a remodeling of the mRNA "translatome" to increase expression of growth-promoting proteins and represents a promising anti-cancer target.

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