OBJECTIVE: Many studies have reported the correlation of microRNAs (miRNAs) with cancers, yet few have proposed the function of miR-150 in gastric cancer. This study intends to discuss the role of miR-150 in gastric cancer development by regulating IRX1. METHODS: Gastric cancer tissues and adjacent tissues were collected. MiR-150-3p, IRX1, CXCL14, and NF-κB (p65) expressions were detected. Gastric cancer cell lines SNU-1 and MKN-45 were used for subsequent cellular experiments. Cell proliferation, colony formation, migration and invasion, apoptosis, and cell cycle distribution in SNU-1 and MKN-45 cells were determined via gain-of and loss-of-function assays. The tumor growth in nude mice was also detected. RESULTS: MiR-150, CXCL14, and NF-κB (p65) were upregulated and IRX1 was downregulated in gastric cancer tissues and cells. CXCL14 and NF-κB (p65) expression was positively related to miR-150 expression and negatively to IRX1 expression. MiR-150 inhibition and IRX1 overexpression in SNU-1 cells restricted viability, colony formation, migration, and invasion abilities, but boosted apoptosis of gastric cancer cells in vitro, and also repressed tumor growth in vivo. These results could be reversed by miR-150 elevation and IRX1 silencing, and the results from in vivo and in vitro experiments were consistent. CONCLUSION: Our study reveals that miR-150 downregulation restrains proliferation, migration, and invasion, while facilitating apoptosis of gastric cancer cells by upregulating IRX1.
OBJECTIVE: Many studies have reported the correlation of microRNAs (miRNAs) with cancers, yet few have proposed the function of miR-150 in gastric cancer. This study intends to discuss the role of miR-150 in gastric cancer development by regulating IRX1. METHODS:Gastric cancer tissues and adjacent tissues were collected. MiR-150-3p, IRX1, CXCL14, and NF-κB (p65) expressions were detected. Gastric cancer cell lines SNU-1 and MKN-45 were used for subsequent cellular experiments. Cell proliferation, colony formation, migration and invasion, apoptosis, and cell cycle distribution in SNU-1 and MKN-45 cells were determined via gain-of and loss-of-function assays. The tumor growth in nude mice was also detected. RESULTS:MiR-150, CXCL14, and NF-κB (p65) were upregulated and IRX1 was downregulated in gastric cancer tissues and cells. CXCL14 and NF-κB (p65) expression was positively related to miR-150 expression and negatively to IRX1 expression. MiR-150 inhibition and IRX1 overexpression in SNU-1 cells restricted viability, colony formation, migration, and invasion abilities, but boosted apoptosis of gastric cancer cells in vitro, and also repressed tumor growth in vivo. These results could be reversed by miR-150 elevation and IRX1 silencing, and the results from in vivo and in vitro experiments were consistent. CONCLUSION: Our study reveals that miR-150 downregulation restrains proliferation, migration, and invasion, while facilitating apoptosis of gastric cancer cells by upregulating IRX1.