Involvement of the long noncoding RNA NEAT1 in carcinogenesis

Abstract

Altered expression levels of the long noncoding RNA (lncRNA) nuclear-enriched abundant transcript 1 (NEAT1) have been reported in different types of cancer. More than half of the NEAT1 studies in cancer have been published within the last 2 years. In this review, we discuss very recent developments and insights into NEAT1 contribution to carcinogenesis. Summarizing the literature, it becomes obvious that NEAT1 is a lncRNA highly de-/upregulated in a variety of cancer entities, in which it primarily acts as a competing endogenous RNA (ceRNA) which sponges tumor-suppressive microRNA (miRNA). The sponged miRNA lose their ability to degrade, silence, or hamper translation of their downstream-mostly oncogenic-target transcripts, ultimately promoting carcinogenesis. This role of NEAT1 function in tumorigenesis suggests it may be a prognostic biomarker as well as potential therapeutic target, pending the completion of further studies into the underlying mechanisms.

Keywords: NEAT1; cancer; ceRNA; lncRNA; miRNA.

Figure 1

Schematic representation of the consequences of elevated NEAT1 expression levels in the context of cancer. (Upper panel) In normal tissue, NEAT1 expression levels are low; therefore, tumor‐suppressive miRNA are not sponged which enables them binding to oncogenic miRNA resulting in a hampered translation and low levels of oncogenic proteins. (Lower panel) In cancer tissue and cancer cell lines NEAT1 expression levels are high. Tumor‐suppressive miRNA are sponged by NEAT1 resulting in reduced binding of these miRNA to oncogenic mRNA. High numbers of these mRNA are translated to oncogenic proteins and cancer cell proliferation, invasion, migration, etc. are promoted.