Lnc-ATB contributes to gastric cancer growth through a MiR-141-3p/TGFβ2 feedback loop
- State Key Laboratory of Bioreactor Engineering & Shanghai Key Laboratory of New Drug Design, School of Pharmacy, East China University of Science and Technology, Shanghai (China)
- School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou, Guangdong PR China (China)
- Department of General Surgery, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai (China)
The long noncoding RNA (lncRNA) ATB is an important regulator in human tumors. Here, we aimed to investigate the potential molecular mechanisms of lnc-ATB in gastric cancer (GC) tumorigenesis. RT-qPCR analysis was used to detect lnc-ATB expression level in 20 pairs of gastric cancer tissues and adjacent normal gastric mucosa tissues (ANTs). Moreover, the biological role of lnc-ATB was determined in vitro. We found that lnc-ATB was significantly upregulated in GC tissues compared to lnc-ATB expression in ANTs. These high lnc-ATB expression levels predicted poor prognosis in GC patients. Low levels of lnc-ATB inhibited GC cell proliferation and cell cycle arrest in vitro. Lnc-ATB was found to directly bind miR-141-3p. Moreover, TGF-β actives lnc-ATB and TGF-β2 directly binds mir-141-3p. Finally, we demonstrated that lnc-ATB fulfilled its oncogenic roles in a ceRNA-mediated manner. Our study suggests that lnc-ATB promotes tumor progression by interacting with miR-141-3p and that Lnc-ATB may be a valuable prognostic predictor for GC. In conclusion, the positive feedback loop of lnc-ATB/miR-141-3p/TGF-β2 may be a potential therapeutic target for the treatment of GC. - Highlights: • Lnc-ATB was up-regulated in GC tissue. • Knockdown of lnc-ATB inhibited proliferation and cell cycle arrest. • The positive feedback loop of lnc-ATB/miR-141-3p/TGF-β2 may be a potential therapeutic target for the treatment of GC.
- OSTI ID:
- 22696899
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 484, Issue 3; Other Information: Copyright (c) 2017 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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