Datasets

Title	Study the global mRNA translation changes between SKBR cells overexpressing VIRMA and eGFP control
Organism
Number of Samples	6
Release Date	2022/06/10 00:00
Sequencing Types
Protocol Details

Title
Authors	Lee Q,Song R,Phan DAV,Pinello N,Tieng J,Su A,Halstead JM,Wong ACH,van Geldermalsen M,Lee BS,Rong B,Cook KM,Larance M,Liu R,Lan F,Tiffen JC,Wong JJ
Journal	Cellular and molecular life sciences : CMLS
Publication Date	2023 May 19
Abstract	Virilizer-like m 6 A methyltransferase-associated protein (VIRMA) maintains the stability of the m 6 A writer complex. Although VIRMA is critical for RNA m 6 A deposition, the impact of aberrant VIRMA expression in human diseases remains unclear. We show that VIRMA is amplified and overexpressed in 15-20% of breast cancers. Of the two known VIRMA isoforms, the nuclear-enriched full-length but not the cytoplasmic-localised N-terminal VIRMA promotes m 6 A-dependent breast tumourigenesis in vitro and in vivo. Mechanistically, we reveal that VIRMA overexpression upregulates the m 6 A-modified long non-coding RNA, NEAT1, which contributes to breast cancer cell growth. We also show that VIRMA overexpression enriches m 6 A on transcripts that regulate the unfolded protein response (UPR) pathway but does not promote their translation to activate the UPR under optimal growth conditions. Under stressful conditions that are often present in tumour microenvironments, VIRMA-overexpressing cells display enhanced UPR and increased susceptibility to death. Our study identifies oncogenic VIRMA overexpression as a vulnerability that may be exploited for cancer therapy. © 2023. The Author(s).
PMC	PMC10198946
PMID	37208522
DOI

Lee et al. 2023 (PRJNA847982)