OBJECTIVE: To uncover the function of LINC00461 in regulating cellular behaviors of gastric cancer (GC) via targeting LSD1. PATIENTS AND METHODS: LINC00461 level in GC tissues with different tumor node metastasis (TNM) staging and lymphatic metastasis statues was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). In vitro influences of LINC00461 on proliferative and apoptotic rates were evaluated in AGS and SGC-7901 cells. The interaction between LINC00461 and LSD1 was explored by RNA immunoprecipitation (RIP) assay and qRT-PCR. Finally, the potential role of LSD1 in the proliferative ability of GC cells mediated by LINC00461 was assessed. RESULTS: LINC00461 level was higher in GC tissues relative to matched control ones. It was positively correlated to TNM staging and lymphatic metastasis of GC. Knockdown of LINC00461 markedly attenuated viability and the proliferative ability of AGS and SGC-7901 cells, but induced apoptosis. RIP assay demonstrated the interaction between LINC00461 and LSD1. Moreover, LSD1 could reverse the regulatory effect of LINC00461 on the proliferative ability of GC cells. CONCLUSIONS: LINC00461 is upregulated in GC, which is positively related to TNM staging and lymphatic metastasis. LINC00461 mediates proliferation and apoptosis of GC cells, thereafter aggravating the progression of GC.
OBJECTIVE: To uncover the function of LINC00461 in regulating cellular behaviors of gastric cancer (GC) via targeting LSD1. PATIENTS AND METHODS: LINC00461 level in GC tissues with different tumor node metastasis (TNM) staging and lymphatic metastasis statues was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). In vitro influences of LINC00461 on proliferative and apoptotic rates were evaluated in AGS and SGC-7901 cells. The interaction between LINC00461 and LSD1 was explored by RNA immunoprecipitation (RIP) assay and qRT-PCR. Finally, the potential role of LSD1 in the proliferative ability of GC cells mediated by LINC00461 was assessed. RESULTS:LINC00461 level was higher in GC tissues relative to matched control ones. It was positively correlated to TNM staging and lymphatic metastasis of GC. Knockdown of LINC00461 markedly attenuated viability and the proliferative ability of AGS and SGC-7901 cells, but induced apoptosis. RIP assay demonstrated the interaction between LINC00461 and LSD1. Moreover, LSD1 could reverse the regulatory effect of LINC00461 on the proliferative ability of GC cells. CONCLUSIONS:LINC00461 is upregulated in GC, which is positively related to TNM staging and lymphatic metastasis. LINC00461 mediates proliferation and apoptosis of GC cells, thereafter aggravating the progression of GC.