Disruption of Long Noncoding RNAs Targets Cancer Hallmark Pathways in Lung Tumorigenesis.

Abstract

Advances in high-throughput genomic and epigenomic technologies have revealed the tremendous complexity of the transcriptional landscape. Beyond protein-coding RNAs (derived from only ∼1.5% of the genome), noncoding RNAs (ncRNA) are emerging as versatile key regulators of gene information involved in multiple major biological processes. Accordingly, deregulation of ncRNA expression has been associated with multiple diseases, including cancer. In this issue of <i>Cancer Research</i>, Shahabi and colleagues characterize <i>LINC00261</i> as a tumor suppressor long ncRNA epigenetically silenced in lung cancer. They provide crucial mechanistic insights to explain its role in lung tumorigenesis, demonstrating that deregulation of the <i>LINC00261</i>/<i>FOXA2</i> locus disrupts DNA damage repair signaling, cell-cycle control, and cell proliferation.<i>See related article by Shahabi et al., p. 3050</i>.