期刊
BIOENGINEERED
卷 13, 期 3, 页码 6978-6995出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/21655979.2022.2037921
关键词
lncRNA MBNL1-AS1; gastric cancer; miR-424-5p; Smad7; TGF-beta/EMT pathways
资金
- Zhejiang Provincial Natural Science Foundation of China [LQ21H160012]
Studies have shown that lncRNA MBNL1-AS1 participates in the progression of gastric cancer by regulating the miR-424-5p/Smad7 axis, thus activating the TGF-beta/EMT pathways. This finding may provide a potential marker for gastric cancer patients.
Studies over the past decades have implicated lncRNAs in promoting the development, migration and invasion of gastric cancer (GC). However, the role and mechanism of lncRNA MBNL1-AS1 in GC promotion are poorly understood. In this research, qRT-PCR showed that MBNL1-AS1 was down-regulated in GC tissues and cells. Cell experiments and the animal study demonstrated that MBNL1-AS1 knockdown accelerated GC cell proliferation, migration, and invasion, thus restraining cell apoptosis. Meanwhile, overexpression of MBNL1-AS1 repressed GC cell promotion. Bioinformatics analysis confirmed that MBNL1-AS1 binds to miR-424-5p via negative modulation. Rescue experiments showed that decreased miR-424-5p level inhibited GC cell promotion by silencing MBNL1-AS1. Furthermore, Smad7 was identified as a target of miR-424-5p that could reverse the promotion of GC cell growth mediated by miR-424-5p. Western blot results proved that MBNL1-AS1 affected TGF-beta/SMAD pathways by regulating the miR-424-5p/Smad7 axis. Collectively, MBNL1-AS1 restrained GC growth via the miR-424-5p/Smad7 axis and thus could be a promising target for GC therapy. These findings illustrate that lncRNA MBNL1-AS1, as a tumor suppressor gene, participates in GC progression by regulating miR-424-5p/Smad7 axis, thus activating TGF-beta/EMT pathways. The evidence may provide a potential marker for GC patients. [GRAPHICS] .
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