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An epitranscriptomic mechanism underlies selective mRNA translation remodelling in melanoma persister cells.

Abstract：

:Cancer persister cells tolerate anticancer drugs and serve as the founders of acquired resistance and cancer relapse. Here we show that a subpopulation of BRAFV600 mutant melanoma cells that tolerates exposure to BRAF and MEK inhibitors undergoes a reversible remodelling of mRNA translation that evolves in parallel with drug sensitivity. Although this process is associated with a global reduction in protein synthesis, a subset of mRNAs undergoes an increased efficiency in translation. Inhibiting the eIF4A RNA helicase, a component of the eIF4F translation initiation complex, abrogates this selectively increased translation and is lethal to persister cells. Translation remodelling in persister cells coincides with an increased N6-methyladenosine modification in the 5'-untranslated region of some highly translated mRNAs. Combination of eIF4A inhibitor with BRAF and MEK inhibitors effectively inhibits the emergence of persister cells and may represent a new therapeutic strategy to prevent acquired drug resistance.

journal_name

Nat Commun

journal_title

Nature communications

authors

Shen S,Faouzi S,Bastide A,Martineau S,Malka-Mahieu H,Fu Y,Sun X,Mateus C,Routier E,Roy S,Desaubry L,André F,Eggermont A,David A,Scoazec JY,Vagner S,Robert C

doi

10.1038/s41467-019-13360-6

subject

Has Abstract

pub_date

2019-12-16 00:00:00

pages

5713

issue

1

issn

2041-1723

pii

10.1038/s41467-019-13360-6

journal_volume

10

pub_type

杂志文章

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