Knockdown of ST7-AS1 inhibits migration, invasion, cell cycle progression and induces apoptosis of gastric cancer.

Role of ST7-AS1 in the malignant progression of gastric cancer (GC) and its molecular mechanisms were investigated. ST7-AS1 level in GC tissues and matched normal tissues was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Its level in GC patients presenting different tumor stages and tumor sizes was determined. Subsequently, ST7-AS1 level in epithelial cells of gastric mucosa and GC cell lines was examined. Cellular behavior of GC cells, including viability, apoptosis, migration, invasion and cell cycle, influenced by ST7-AS1 was evaluated. The interaction between ST7-AS1 and EZH2 was assessed by RNA immunoprecipitation (RIP) assay. The involvement of EZH2 in the progression of GC mediated by ST7-AS1 was identified. ST7-AS1 was upregulated in GC tissues and cell lines. Its level was positively correlated to tumor stage and tumor size of GC. Knockdown of ST7-AS1 attenuated proliferative, migratory and invasive abilities, arrested cell cycle progression and induced apoptosis of GC cells. EZH2 was identified to interact with ST7-AS1, which attenuated the regulatory effects of ST7-AS1 on migratory and invasive abilities of GC cells. Upregulated ST7-AS1 in GC accelerated proliferation, migration and invasion, and inhibited apoptosis, thus aggravating the progression of GC.
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