1.3.2 CeRNA
Competitive endogenous RNA (ceRNA) reveals a novel role of RNA-RNA
interaction, which has been heavily studied in recent years. At the
post-transcriptional level, miRNA attaches to the miRNA response element
(MRE) at the 3’-UTR end of the target gene and suppresses translation.
While certain lncRNAs produce MREs as well as function as miRNA sponges,
competing to other targeted mRNAs. The ceRNA mechanism refers to the
competitive binding between lncRNAs and mRNAs[17]. Other RNAs, such
as mRNA, pseudogenes, and circRNA also can serve in this way as
ceRNA[18].
LncRNA Sox2ot from exosomes derived from highly invasive tumor cells,
binding to miR-200 as ceRNA mechanism, upregulate Sox2, to induce
epithelial-mesenchymal transition (EMT) and stem cell like properties in
different tumor cells, plays important roles in pancreatic ductal
adenocarcinoma invasion and metastasis[19]. Lnc SNHG1 promote
neuroinflammation, and neuronal toxicity via different mechanisms,in
the process of Alzheimer’s disease, it could act as ceRNA for miR-137,
targeting KREMEN1 in the human primary neuron (HPN) cells, reduce cell
viability, promote cell apoptosis, decrease mitochondrial membrane
potential and the protein levels of cytochrome C[20].
Whereas, there are some reports claiming that ceRNA only performs a
slight role in miRNA regulation, single ceRNA is unlikely to have any
biologically significant effects on the activity of miRNAs, or the
expression of genes[11, 21]. Most of RBP and miRNAs regulate gene
expression post-transcriptional have thousands of binding sites, the
numbers of these binding sites are highly dynamic as transcription
renders, only strong binding sites are likely to be altered by this
crosstalk effect[22].
1.3.3 LncRNA
co-expresses with miRNA as a pri-miRNA
Some miRNAs host genes can encode both lncRNA and miRNA, one of the
functions of this class of lncRNAs is to act as primary miRNA, termed
lnc-pri-miRNAs, able to produce miRNAs[23]. Among them, lnc
LOC646329 can act as both a pri-miRNA to produce miR-29a/b1, and a
transcriptional enhancer to activate neighboring oncogenes and promote
Glioblastoma cell proliferation[24]. The genomic organization of lnc
MIR100HG, is located on human chromosome 11 (hsa chr11),generate
miR-100 and miR-125b,which co-represses several Wnt/β-catenin negative
regulators,to rescue cetuximab responsiveness of cetuximab-resistant
colorectal cancer and head and neck squamous cell cancer cell
lines[25].