Taurine‐upregulated gene 1: A functional long noncoding RNA in tumorigenesis

Taurine‐upregulated gene 1 (TUG1) is a 7.1 kb long noncoding RNA (lncRNA) first recognized in 2005 as an important element for retinal development in rodents. Subsequently, this lncRNA has been shown to participate in oncogenic processes through alteration in chromatin structure, sponging microRNAs,...

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Veröffentlicht in:Journal of cellular physiology 2019-10, Vol.234 (10), p.17100-17112
Hauptverfasser: Ghaforui‐Fard, Soudeh, Vafaee, Reza, Taheri, Mohammad
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Sprache:eng
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Zusammenfassung:Taurine‐upregulated gene 1 (TUG1) is a 7.1 kb long noncoding RNA (lncRNA) first recognized in 2005 as an important element for retinal development in rodents. Subsequently, this lncRNA has been shown to participate in oncogenic processes through alteration in chromatin structure, sponging microRNAs, and affecting the expression of some cancer‐related pathways. While most of the studies have revealed an oncogenic role for this lncRNA, some reports have shown downregulation of TUG1 in lung cancer samples compared with noncancerous samples. In triple negative breast cancer samples, the expression of this lncRNA has been decreased. Besides, its expression has been higher in HER2‐enriched and basal‐like subtypes compared with luminal A. In the current review, we discuss the latest literature about the expression pattern and functional roles of TUG1 in diverse cancer types. In addition, its role in epithelial−mesenchymal transition and activation of Wnt/β‐catenin pathway in human malignancies will be explored. Taurine‐upregulated gene 1 (TUG1) exert its roles in the tumorigenesis process through different mechanisms: (a) through epigenetic mechanisms and by recruitment of polycomb repressive complex 2 (PRC2) suppresses the expression of the tumor suppressor KLF2. (b) Through suppression of miR‐145 and its effects on Sirt3/GDH influences the cancer course: Sirt3 expression in tumoral cells is associated with lower levels of reactive oxygen species (ROS) production, maintenance of adenosine triphosphate (ATP)/energy levels and upregulation of antiapoptotic proteins such as BCL2. GDH facilitates epithelial−mesenchymal transition (EMT). TUG1 inhibits miR‐145 and subsequently suppresses MYC and SOX2 degradation. (c) Through inhibition of miR‐142‐3p, affect the expression of ZEB1 and EMT process. (d) Through inhibition of miR‐142‐3p affect the expression of ZEB2 and activation of Wnt/β‐catenin pathway.
ISSN:0021-9541
1097-4652
DOI:10.1002/jcp.28464