This study found that THUMPD3-AS1 is upregulated in gastric cancer and is significantly correlated with poor prognosis. Functionally, THUMPD3-AS1 promotes proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of gastric cancer cells and induces tumor growth in vivo. THUMPD3-AS1 exerts its regulatory function on BCAT1 through competitive binding with miR-1297.
Long noncoding RNA (lncRNA) plays crucial roles in the development of gastric cancer (GC); however, studies of their mechanisms of action are needed to determine their clinical value. The aim of this study is to explore the effects and mechanisms of THUMPD3-AS1 in GC. Elevated levels of THUMPD3-AS1 were observed in GC and demonstrated a significant positive correlation with poor prognosis. Functionally, THUMPD3-AS1 promoted GCcell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) and induced tumor growth in vivo. THUMPD3-AS1 exerts its regulatory function on BCAT1 through competitive binding with miR-1297. Further investigations confirmed that both THUMPD3-AS1 and miR-1297 interact with BCAT1. These findings suggest that THUMPD3-AS1 promotes GC invasion and EMT by regulating the miR-1297/BCAT1 pathway, indicating that THUMPD3-AS1 may serve as a biomarker and therapeutic target for GC.
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