期刊
AGING-US
卷 13, 期 23, 页码 25138-25152出版社
IMPACT JOURNALS LLC
关键词
gastric cancer; SNHG3; miR-139-5p; MYB
资金
- National Natural Science Foundation of China [81802437]
- Key Research and Development of Social and People's Livelihood [cstc2018jscx-mszdX0031]
- Chongqing medical scientific research project (Chongqing Health Commission) [2022GDRC019]
- Chongqing medical scientific research project (Science and Technology Bureau) [2022GDRC019]
High expression of SNHG3 in gastric cancer is correlated with tumor clinical stage and patient survival rate, while knocking down SNHG3 can inhibit the proliferation, migration, and invasion of GC cells. SNHG3 binds and sequesters miR-139-5p to indirectly promote the upregulation of the miR139-5p target gene MYB, driving the oncogenic activities of GC.
The long non-coding RNA (lncRNA) SNHG3 has been shown to play oncogenic roles in several cancer types, but the mechanisms underlying its activity are poorly understood. In this study, we aimed to explore the clinical relevance and mechanistic role of SNHG3 in gastric cancer (GC). We found that SNHG3 expression in GC cell lines and tissues was significantly increased, and the upregulation of this lncRNA was correlated with tumor clinical stage and decreased patient survival. Knocking down SNHG3 in GC cells impaired the proliferative, migratory, and invasive activity in vitro and constrained in vivo GC xenograft tumor growth. Mechanistically, SNHG3 was found to bind and sequester miR-139-5p, thereby indirectly promoting the upregulation of the miR139-5p target gene MYB. These data demonstrated that SNHG3 functions in an oncogenic manner to drive GC proliferation, migration, and invasion by regulating the miR-139-5p/MYB axis.
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