SNHG17 promotes gastric cancer cell proliferation and invasion by suppressing RUNX3 via interacting with EZH2

• Autor(a) principal: ZHANG,Xinmei
• Data de Publicação: 2022
• Outros Autores: FAN,Guofang, ZHAN,Jianghong, GUAN,Zihua
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Food Science and Technology (Campinas)
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-20612022000100730
• topic: gastric cancer; long noncoding RNAs; SNHG17; EZH2; RUNX3

Abstract Accumulating data has indicated that long noncoding RNAs (lncRNAs) play critical roles in multiple cancers including gastric cancer (GC). However, the functional role of SNHG17 in gastric cancer (GC) development and related biological mechanisms remain unknown. In the study, our results demonstrated that SNHG17 expression was higher in tumor tissues compared to adjacent normal tissues in 99 cases of patients with GC. Higher SNHG17 expression positively associated with lymph node metastasis, advanced TNM stage and predicted a worse prognosis in GC patients. Functionally, we showed that overexpression of SNHG17 promoted cell proliferation, cell colony formation and cell invasion in vitro. However, SNHG17 knockdown significantly inhibited cell proliferation and invasion of GC. Furthermore, we demonstrated that SNHG17 promoted cell proliferation and invasion by regulating RUNX3 via interacting with EZH2 in GC cells. In addition, overexpression of SNHG17 reversed the cell proliferation and invasion induced by SNHG17 in GC. Thus, these results indicated that SNHG17 could serve as a prognostic biomarker and target of GC treatment.