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Key role of dysregulated SF3A3 translation in MYC-induced breast tumorigenesis

ABSTRACT: Key role of dysregulated SF3A3 translation in MYC-induced breast tumorigenesis

PROVIDER: PRJNA615004 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11411712.fastq.gz	Fastqsanger.gz
	SRR11411713.fastq.gz	Fastqsanger.gz
	SRR11411714.fastq.gz	Fastqsanger.gz
	SRR11411715.fastq.gz	Fastqsanger.gz
	SRR11411716.fastq.gz	Fastqsanger.gz

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RNA-seq analysis in fibroblast IMR90 CTRL/MYC/MYC+SF3A3 KD

Project description:Splicing is a central RNA-based process commonly altered in human cancers; however, how the splicing machinery is co-opted during tumorigenesis remains largely unresolved. Here we identify the splice factor SF3A3 at the nexus of an oncogenic translation program that rewires splicing to promote tumorigenesis. Our results suggest that key spliceosomal networks centered on the essential core U2-associated factor, SF3A3, are exquisitely controlled at the translation level during oncogenic stress. Upon oncogene activation, SF3A3 translation is rapidly enabled via a conserved internal stem-loop structure embedded in the transcript 5’ untranslated region (UTR). Uncoupled SF3A3 translation leads to alternative splicing of several mRNAs involved in mitochondrial dynamics, and induces a metabolic switch that fuels cancer initiation properties in MYC-driven breast tumorigenesis in vivo. Finally, we compelling show that SF3A3 is post-transcriptionally altered and predicts for poor prognosis in aggressive triple negative breast cancers. Together, these findings unveil a highly dynamic regulatory network that interfaces mRNA splicing and translation to orchestrate cancer gene expression networks.

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Key role of dysregulated SF3A3 translation in MYC-induced breast tumorigenesis

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

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Targeted DMS probing of SF3A3 5' UTR

Project description:To delineate the native structure of SF3A3 5'UTR, RNA was harvested from IMR90 human fibroblasts. Using specific primers and DMS-MaPSeq pipeline, we validated individual base pairing probabilities within the endogenous 5'UTR of SF3A3 (samples described as 'in vivo' transcribed). DMS-MaP-Seq is based on the principle that DMS is highly reactive to solvent-accessible, unpaired adenine (A) and cytosine (C) residues, but remains inert toward base-paired A and C engaged in Watson-Crick interactions (Rouskin et al., 2014). Using this methodology, we identify stable stem-loop structure (SL3) positioned within SF3A3 5'UTR. To further validate the functional importance of SL3, the structural point mutant (SF3A3 5'UTR mut: A55C and U95A) and rescue (SF3A3 5'UTR res: A55C and U95A and rescuing point mutations G61U and U100G) sequences of SF3A3 5'UTR were cloned into the reporter plasmid. For the validation of these mutate-and-rescue constructs, plasmids were in vitro transcribed and either used directly (samples described as 'in vitro') for DMS-MaP-Seq probing.

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RNA-seq analysis in fibroblast IMR90 CTRL/MYC/MYC+SF3A3 KD

Project description:RNA-seq analysis in fibroblast IMR90 CTRL/MYC/MYC+SF3A3 KD

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ALKBH8-Mediated Codon-Specific Translation Promotes Colorectal Tumorigenesis

Project description:Reprogramming gene expression at the translational level drives intestinal tumorigenesis. Codon decoding during translation elongation relies on tRNA modifications, while their pathological relevance in colorectal cancer remains to be elucidated. Here, we show that AlkB homolog 8 (ALKBH8), a uridine 34 (U34) tRNA methyltransferase, is a direct target of Wnt/β-catenin and is upregulated in colorectal cancer. Genetic ablation of ALKBH8 inhibits the development of intestinal tumors in Apcmin/+, AOM/DSS, and xenograft models. Loss of ALKBH8 induces ribosome pausing at adenine-ending codons, impairing the translation elongation of mRNAs enriched with these codons. Specifically, ALKBH8 regulates the translation of KRAS proto-oncogene in a codon-dependent manner. Rescue experiments demonstrate that the methyltransferase activity of ALKBH8 is required for its translation-promoting function. Together, our findings reveal ALKBH8-dependent mRNA translation as a critical mediator of intestinal tumorigenesis, underscoring its potential as a promising target for colorectal cancer therapy.

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