Long Noncoding Competing Endogenous RNA Networks in Pancreatic Cancer

Abstract

Pancreatic cancer (PC) is a highly malignant disease characterized by insidious onset, rapid progress, and poor therapeutic effects. The molecular mechanisms associated with PC initiation and progression are largely insufficient, hampering the exploitation of novel diagnostic biomarkers and development of efficient therapeutic strategies. Emerging evidence recently reveals that noncoding RNAs (ncRNAs), including long ncRNAs (lncRNAs) and microRNAs (miRNAs), extensively participate in PC pathogenesis. Specifically, lncRNAs can function as competing endogenous RNAs (ceRNAs), competitively sequestering miRNAs, therefore modulating the expression levels of their downstream target genes. Such complex lncRNA/miRNA/mRNA networks, namely, ceRNA networks, play crucial roles in the biological processes of PC by regulating cell growth and survival, epithelial-mesenchymal transition and metastasis, cancer stem cell maintenance, metabolism, autophagy, chemoresistance, and angiogenesis. In this review, the emerging knowledge on the lncRNA-associated ceRNA networks involved in PC initiation and progression will be summarized, and the potentials of the competitive crosstalk as diagnostic, prognostic, and therapeutic targets will be comprehensively discussed.

Keywords: competing endogenous RNA; long noncoding RNA; microRNA; network; pancreatic cancer.

Figure 1

The lncRNA mediated ceRNA mechanism and the identified lncRNA/miRNA/mRNA networks in several hallmarks of PC. lncRNA, long noncoding RNA; ceRNA, competitive endogenous RNA; miRNA, microRNA; mRNA: mRNA, messenger RNA; PC, pancreatic cancer; EMT, epithelial-mesenchymal transition.