Conclusions
TOB1-AS1/miR-23a/NEU1 axis regulated proliferation, apoptosis, migration, and invasion of GC cells via Wnt/b-catenin pathway, providing the evidence for serving TOB1-AS1 as an underlying therapeutic target in human GC treatment.
Methods
We collected 21-paired GC and para-carcinoma tissue specimens, and the levels of TOB1-AS1 and lysosomal sialidase (NEU1) were detected by quantitative Real-Time Polymerase Chain Reaction (qRT-PCR). The protein expression levels of NEU1, b-catenin, c-Myc, Cyclin D1, N-cadherin were determined via Western blot. Cell proliferation was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Flow cytometry was performed to evaluate cell proliferation. Besides, GC cell migration and invasion capacities were identified by transwell assay. Dual-Luciferase reporter assay was employed to examine the interrelation between miR-23a and TOB1-AS1 or NEU1. Finally, the role of TOB1-AS1 was verified in vivo.
Objective
Gastric cancer (GC) is the fourth common cancer worldwide. Long non-coding RNA TOB1 antisense RNA 1 (TOB1-AS1) has been found to participate in the process of GC, while the precise role of TOB1-AS1 is still not understood in GC progression. Materials and
Results
The levels of TOB1-AS1 were decreased in GC tissues and cell lines. Either TOB1-AS1 or NEU1 upregulation accelerated GC cell apoptosis, hampered proliferation, migration, and invasion. Further, the role of TOB1-AS1 silencing on cell behaviors was abrogated by NEU1 upregulation. TOB1-AS1 and NEU1 exerted their roles via Wnt/b-catenin signaling pathway. Overexpression of TOB1-AS1 blocked GC development in vivo. Mechanically, miR-23a was targeted by TOB1-AS1, but directly targeted NEU1. Conclusions: TOB1-AS1/miR-23a/NEU1 axis regulated proliferation, apoptosis, migration, and invasion of GC cells via Wnt/b-catenin pathway, providing the evidence for serving TOB1-AS1 as an underlying therapeutic target in human GC treatment.