TUG1 as a Therapy Target in Pancreatic Cancer
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TUG1 as a Therapy Target in Pancreatic Cancer Haifeng Liang1 · Zhaokun Cui2 · Qingping Song3 Received: 14 August 2020 / Accepted: 22 September 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
To the Editors, I read with interest the article by Xu et al. [1] revealing that long noncoding RNA (lncRNA) taurine-upregulated gene 1 (TUG1) is upregulated in pancreatic cancer (PC) tissues and cells. They further show that TUG1 knockdown inhibited cell proliferation, invasion, migration, and epithelial–mesenchymal transition (EMT), and induced apoptosis in PC cells by sponging miR-299-3p via suppressing the Notch1 pathway. The results indicate that the TUG1/miR-299-3p/Notch1 pathway is important for the development of PC, which may have therapeutic potential for patients with PC. Although this novel discovery opens the door to new treatments for PC, it is not known whether TUG1 deficiency or inhibition suppresses the development of PC only through interfering with the miR-299-3p/Notch1 pathway and whether genetic deletion or pharmaceutical inhibition of TUG1 could produce unwanted side effects. Note that data reported from animal studies demonstrated a similar function of TUG1. One study demonstrated that knockdown of TUG1 significantly inhibited renal cell carcinoma formation in vitro and in vivo by modulating the TUG1/miR-299-3p/VEGFA axis [2]. Another study showed that TUG1 promoted gallbladder carcinoma (GBC) proliferation, metastasis, and EMT progression by negative modulation of miR-300. The TUG1/miR-300 signaling pathway may be a novel therapeutic target for GBC [3]. Along this line, it would be interesting to determine whether targeting TUG1 suppresses development of PC through the miR299-3p/VEGFA axis and miR-300 pathway. Therefore, more * Qingping Song [email protected] 1
Department of Surgery, Liaocheng Cancer Hospital, Liaocheng 252000, People’s Republic of China
2
Department of Anesthesia and Surgery Center, Liaocheng Cancer Hospital, Liaocheng 252000, People’s Republic of China
3
Department of Thoracic Surgery, Liaocheng Cancer Hospital, Liaocheng 252000, People’s Republic of China
studies should be performed to explore the mechanism of TUG1 in PC. Fang et al. [4] observed that TUG1 inhibition induced cardiomyocyte hypertrophy and that TUG1 overexpression alleviated cardiomyocyte hypertrophy by regulation of miR34a expression. These observations demonstrate that TUG1 may serve as a novel molecular target for treating cardiac hypertrophy. More importantly, a previous study demonstrated that overexpression of TUG1 protected cells from inflammatory injury induced by lipopolysaccharide via regulating miR-223 and Sirt1 expression, as well as modulating PI3K/AKT and NF-κB signaling. This study suggested that TUG1 acted as a protective factor in lupus nephritis [5]. For clinical application, the desired approach is to modulate TUG1 expression to treat PC without inducing unwanted side effects in other organs. Thus, it would be interesting to know whether the ant
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