Abstract

Background: Long non-coding ribonucleic acid (lncRNA) are known as similar transcripts of messenger RNA (mRNA) whose size discrepancy is between 100 and 200 nucleotides. Recent studies in this area have revealed that lncRNAs are involved in cancer tumorigenesis and progression. Such molecules are transcribed from genome regions that lack open reading frame (ORF) and fail to encode any protein. LncRNAs are characterized by tumorigenic behaviors, which can be considered as new biomarkers. Among all types of thyroid cancer (TC), papillary thyroid carcinoma (PTC) is the most common one.

Methods: This review was prepared via searching of the databases of Science Direct, Directory of Open Access Journals (DOAJ), Google Scholar, Pub-Med (NLM), Scopus, Web of Science, and hand searching using relative keywords. The selected papers were fully reviewed and the required information for the review was extracted and summarized.

Results: Previous studies indicated that BRAF-activated non-protein coding RNA (BANCR) expression had been increased in thyroid tumors compared with adjacent normal tissues. Additionally, BANCR had mediated epithelial-mesenchymal transition (EMT) through regulating the expression of epithelial (E)-cadherin, vimentin, and neuronal (N)-cadherin. Moreover, H19 was an example of a lncRNA that could function either as a tumor promoter or suppressor. An important part of this study was dedicated to reviewing signaling pathways involved in TC including extracellular-signal-regulated kinase (ERK) pathway and mitogen-activated protein kinase (ERK/MAPK), transforming growth factor-β/ (TGF-ß)/Smads, the Janus kinase/signal transducers and activators of transcription (JAK/STAT), P53, as well as other pathways.

Conclusion: Briefly, this study provided an overview of the current understanding of the function of lncRNA and micro RNAs (miRNAs) along with their interactions in TC.

Keywords: Long Non-Coding RNA, Thyroid Cancer, Signaling Pathway, papillary thyroid carcinoma, H19, extracellularsignal- regulated kinase.