Abstract
Previously thought of as junk transcripts and pseudogene remnants, long non-coding RNAs (lncRNAs) have come into their own over the last decade as an essential component of cellular activity, regulating a plethora of functions within multicellular organisms. lncRNAs are now known to participate in development, cellular homeostasis, immunological processes, and the development of disease. With the advent of next generation sequencing technology, hundreds of thousands of lncRNAs have been identified. However, movement beyond mere discovery to the understanding of molecular processes has been stymied by the complicated genomic structure, tissue-restricted expression, and diverse regulatory roles lncRNAs play. In this review, we will focus on lncRNAs involved in lung cancer, the most common cause of cancer-related death in the United States and worldwide. We will summarize their various methods of discovery, provide consensus rankings of deregulated lncRNAs in lung cancer, and describe in detail the limited functional analysis that has been undertaken so far.
Highlights
The pace of discovery and functional validation for long non-coding RNAs (lncRNAs) has been increasing exponentially with the advent of sequencing technologies (Figure 1)
Because lncRNAs were grouped into a broad category of any non-coding RNA longer than 200 nucleotides, this class of RNAs represents a heterogeneous group in terms of mechanism and function. lncRNAs are implicated in transcriptional regulation, cellular signaling, chromatin remodeling, splicing, and a host of other processes [22,23,24,25]
RP11-57A19.2 is transcribed in an antisense direction from the SBK1 promoter, and the two have correlated expression in multiple cancer types (TCGA-Lung adenocarcinoma (LUAD) R=0.597, The Cancer Genome Atlas (TCGA)-OVR=0.701, TCGABRCA=0.671, p=3.95e-108 [143]), little to nothing is known about the expression, function, and regulation of RP11-57A19.2
Summary
The pace of discovery and functional validation for lncRNAs has been increasing exponentially with the advent of sequencing technologies (Figure 1). The established mechanism of action is listed, as well as other cancers where the lncRNA has demonstrated effects on tumor initiation, promotion, progression, and/or patient survival outcomes. Multiple functions for MEG3 in cancer have been described [87, 88], Locally, expression is inversely correlated with the nearby tumor suppressor DLK1, which it may regulate [89].
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