Knockdown of SETD5 inhibited glycolysis and tumor growth in gastric cancer cells by down-regulating Akt signaling pathway

Abstract

Abstract Gastric cancer (GC) is the 5th most common cancer and the 3rd leading cause of cancer-related death worldwide. It is of great significance to study the underlying molecular mechanism of GC, and targeting glycolysis is a good strategy to treat GC. SET domain containing 5 (SETD5) contains a catalytic methyltransferase SET domain, which is known as a lysine methyltransferase that affects the progression of multiple cancers. However, its possible role in GC was still unclear. Here, we revealed that SETD5 was highly expressed in GC and was associated with a poor prognosis. Further through the in vitro experiments, we revealed that the downregulation of SETD5 inhibited the proliferation and migration of GC cells. Knockdown of SETD5 inhibited glucose consumption and glycolysis. Further studies have shown that SETD5 knockdown restrained the Akt signaling pathway. Therefore, we thought that SETD5 could act as a GC target.