小RNA
生物
癌基因
细胞生物学
机制(生物学)
功能(生物学)
衰老
信号转导
长非编码RNA
非编码RNA
抗凋亡Ras信号级联
核糖核酸
计算生物学
遗传学
癌症
基因
细胞周期
MAPK/ERK通路
认识论
哲学
作者
Bing Shui,Gaspare La Rocca,Andrea Ventura,Kevin M. Haigis
标识
DOI:10.1016/j.trecan.2022.01.002
摘要
K-RAS is frequently mutated in cancers, and its overactivation can lead to oncogene-induced senescence (OIS), a barrier to cellular transformation. Feedback onto K-RAS limits its signaling to avoid senescence while achieving the appropriate level of activation that promotes proliferation and survival. Such regulation could be mediated by miRNAs, as aberrant RAS signaling and miRNA activity coexist in several cancers, with miRNAs acting both up- and downstream of K-RAS. Several miRNAs both regulate and are regulated by K-RAS, suggesting a noncoding RNA-based feedback mechanism. Functional interactions between K-RAS and the miRNA machinery have also begun to unfold. This review comprehensively surveys the state of knowledge connecting K-RAS to miRNA function and proposes a model for the regulation of K-RAS signaling by noncoding RNAs.
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