TINCR: An lncRNA with dual functions in the carcinogenesis process

Abstract

Long non-coding RNAs (lncRNAs) have prominent roles in the pathogenesis of human cancers. Several studies have shown oncogenic or tumor suppressor roles of lncRNAs in different human tissues. Thus, these transcripts have been regarded as putative targets in treatment of cancer. The lncRNA terminal differentiation-induced non-coding RNA (TINCR) has an especial position in this regard, as it exerts different opposite roles in the pathogenesis of different human cancers. While it is up-regulated in gastric, esophageal, bladder and breast cancer; it is down-regulated in glioma, retinoblastoma and prostate cancer. Notably, data regarding expression profile of this lncRNA in a number of human cancers such as colon cancer, squamous cell carcinoma, non-small cell lung cancer (NSCLC) and hepatocellular carcinoma (HCC) are controversial. Expression level of this lncRNA has been associated with clinical outcome in patients with gastric cancer, colorectal cancer, NSCLC and head and neck squamous cell carcinoma. Moreover, Kaplan-Meier analyses have shown correlation between expression levels of TINCR and patients survival in patients with lung cancer and HCC. A number of cellular pathways such as Wnt/β-catenin, ERK1/2‐SP3 and MAPK signaling pathways have been identified as targets of this lncRNA in different cancers. Moreover, the rs8113645, rs2288947 and rs8105637 within this lncRNA have been associated with risk of gastric and colorectal cancer. In conclusion, although the role of TINCR in the carcinogenesis is essential, based on the conflicting data regarding the direction of effect of this lncRNA, therapeutic targeting of this lncRNA is a complicated issue which should be considered in a tissue-specific or even individualized manner.

A ubiquitin-like protein encoded by the “noncoding” RNA TINCR promotes keratinocyte proliferation and wound healing

“…The abundance of TINCR is up-regulated in various cancers, in which it promotes proliferation of the cancer cells [ 10 – 21 ]. In the present study, we found that forced expression of TUBL promoted keratinocyte proliferation in a manner independent of the RNA secondary structure of TINCR, suggesting that promotion of cancer cell proliferation by TINCR is also likely mediated by TUBL protein rather than by TINCR RNA.…”

“…These mRNAs interact with TINCR via a 25-nucleotide (nt) motif known as the TINCR box and appear to be stabilized by the TINCR-STAU1 complex. Recent studies have also revealed a role for TINCR in cancer, including breast, lung, liver, esophageal, colon, bladder, prostate, gastric, and oral tumors [ 10 – 21 ]. Forced expression of TINCR promotes cell proliferation and metastasis through activation of the Wnt/β-catenin signaling pathway in oral squamous cell carcinoma [ 20 ].…”

Long Non-Coding RNAs as Potential Diagnostic and Prognostic Biomarkers in Breast Cancer: Progress and Prospects

“…Aberrant TINCR expression has been implicated in multiple human cancers. TINCR expression is upregulated in gastric, gladder and breast cancer but downregulated in glioma and prostate cancer ( 208 ). In recent years, several studies have been performed on the contribution of TINCR to breast cancer.…”

Long noncoding RNA DLGAP1-AS1 promotes the progression of glioma by regulating the miR-1297/EZH2 axis

“…Long noncoding RNAs (lncRNAs) are a non-protein coding section of the genome measuring approximately 200 nucleotides in length [ 6 , 7 ]. These molecules can regulate expression of genes at the apparent, transcriptional, and post-transcriptional levels through a variety of interactions between DNA, RNA and proteins [ 8 , 9 ]. These molecules have received much attention with regards to their role in the initiation and development of several diseases.…”