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miR4673 improves fitness profile of neoplastic cells by induction of autophagy.

Abstract：

:Therapeutic resistance of neoplasms is mainly attributed to gradual evolution of mutational profile1. Here, we demonstrate a microRNA-mediated mechanism that effectively improves fitness of SKBR3 mammary carcinoma cells by cytoplasmic reprogramming. The reprogramming is triggered by endogenous miR4673 transcribed from notch-1 locus. The miRNA downregulates cdk-18, a cyclin-dependent kinase that regulates M-G1 transition in cycling cells2,3. Suppression of cdk-18 triggers mitophagy and autophagy. Due to high autophagic flux, oestrogen receptor-1+/progesterone receptor+/p53+ (Esr1+/Pr+/p53+) SKBR3 cells are coerced into an Esr1-/Prlow/p53-profile. Increased mitophagy in combination with proteasomal degradation of p53 transiently arrests the cycling cells at G0 and enhances radio-resistance of the SKBR3 population. These findings highlight the impact on cancer therapy of non-encoded neoplastic resistance, arising as a consequence of miRNA-mediated autophagic reprogramming that uncouples phenotype and genotype.

journal_name

Cell Death Dis

journal_title

Cell death & disease

authors

Dökümcü K,Simonian M,Farahani RM

doi

10.1038/s41419-018-1088-6

subject

Has Abstract

pub_date

2018-10-19 00:00:00

pages

1068

issue

11

issn

2041-4889

pii

10.1038/s41419-018-1088-6

journal_volume

9

pub_type

杂志文章

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