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Induction of DISE by tumor suppressive microRNAs

ABSTRACT: Induction of DISE by tumor suppressive microRNAs

PROVIDER: PRJNA436738 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6799610.fastq.gz	Fastqsanger.gz
	SRR6799620.fastq.gz	Fastqsanger.gz
	SRR6799611.fastq.gz	Fastqsanger.gz
	SRR6799621.fastq.gz	Fastqsanger.gz
	SRR6799612.fastq.gz	Fastqsanger.gz

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Induction of DISE by tumor suppressive microRNAs

Project description:Many siRNAs and shRNAs induce a form of cell death in all cancer cells by silencing a set of critical survival genes in a process called death induced by survival gene elimination (DISE). Mechanistically, a 6mer seed sequence (position 2-7 of the guide strand) is sufficient to confer DISE-inducing activity. We have now performed a strand-specific screen testing the toxicity of all 4096 possible 6mer seed sequences in a neutral double-stranded siRNA backbone. We found an asymmetric preference for guanine in positions 1-3 and a G content of >80% of the 6mer seed in the most toxic siRNAs, which target survival genes that are GC rich in their 3'UTR. During over 800 million years of evolution, miRNAs have evolved to avoid guanine in their seed sequences. However, two tumor suppressive miRNAs were found to be killing cancer cells through DISE using G rich toxic 6mer seeds in cells exposed to genotoxic stress: 1) the p53 inducible miR-34 family; and 2) miR-320a, a noncanonical miRNA that is still expressed in cancer cells when miRNA processing genes are mutated. Our data suggest that most miRNAs have evolved to avoid induction of DISE but certain tumor suppressive miRNAs utilize this mechanism to kill cancer cells.

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Project description:microRNA dysregulation is a common feature of cancer cells, but the complex roles of microRNAs in cancer are not fully elucidated. Here we used functional genomics to identify oncogenic microRNAs in non-small cell lung cancer and to evaluate their impact on response to EGFR targeting therapy. Our data demonstrate that microRNAs with an AAGUGC-motif in their seed-sequence increase both cancer cell proliferation and sensitivity to EGFR inhibitors. Global transcriptomics, proteomics and target prediction resulted in the identification of several tumor suppressors involved in the G1/S transition as targets of AAGUGC-microRNAs. The clinical implications of our findings were evaluated by analysis of public domain data supporting the link between this microRNA seed-family, their tumor suppressor targets and cancer cell proliferation. In conclusion we propose that AAGUGC-microRNAs are an integral part of an oncogenic signaling network, and that these findings have potential therapeutic implications, especially in selecting patients for EGFR-targeting therapy.

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