Journal
ONCOLOGY RESEARCH
Volume 26, Issue 7, Pages 1063-1072Publisher
TECH SCIENCE PRESS
DOI: 10.3727/096504018X15152072098476
Keywords
Bladder cancer; MicroRNA-126; KRAS; PI3K/AKT/mTOR; Long noncoding RNA activated by transforming growth factor-beta (lncRNA-ATB)
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This study aimed to explore the biological functions of long noncoding RNA activated by transforming growth factor-beta (lncRNA-ATB) in bladder cancer cells. For the expressions of lncRNA-ATB, miR-126, and KRAS, T24 cells were transfected with their specific vectors/shRNA or mimic/inhibitor. Then cell viability, migration, invasion, and apoptosis as well as the protein levels of apoptosis-related factors and PI3K/AKT and mTOR signal pathways were measured. The relationships of lncRNA-ATB and miR-126 or miR-126 and KRAS were analyzed by Dual-Luciferase Reporter assay. Functional experiments showed that lncRNA-ATB overexpression significantly promoted cell viability, migration, and invasion in T24 cells. lncRNA-ATB was a molecular sponge of miR-126 and exerted tumor-promoting effects by downregulation of miR-126. Moreover, KRAS was a direct target of miR-126 and was negatively regulated by miR-126. Finally, overexpression of KRAS increased cell viability, migration, and invasion, as well as activated PI3K/AKT and mTOR signaling pathways in T24 cells. The results revealed that lncRNA-ATB was an oncogene, which promoted cell proliferation, migration, and invasion by regulating miR-126 in bladder cancer. These findings may provide a potential prognostic biomarker and a therapeutic target for bladder cancer.
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