Geniposide suppresses growth, migration and invasion of MKN45 cells by down-regulation of lncRNA HULC.

Gastric cancer (GC) is a serious disease with high incidence rate and high mortality. Geniposide (GEN) exhibits multiple biological properties including anti-tumor function. However, effect of GEN on GC is not well studied. Hence, the effects of GEN on GC were investigated in our study. HULC expression in GC tissue and GC cell lines (MKN45, SGC-7901, MKN28, AGS) was detected by qRT-PCR. Cell viability, colony formation, migration, invasion and cell apoptosis were examined by CCK-8 assay, survival fraction assay, modified two-chamber migration assay, Millicell Hanging Cell Culture and flow cytometry analysis, respectively. The expression of matrix metalloproteinase (MMP)-2/9 and vimentin was detected by qRT-PCR and western blot, respectively. The expression of PI3K/AKT and JNK was measured by western blot. The expression of HULC was up-regulated both in GC tissue and cell lines (P < .05, P < .01 or P < .001). GEN negatively regulated the expression of HULC in MKN45 cells (P < .05 or P < .01). GEN decreased cell viability (P < .05), colony formation (P < .01), migration (P < .05) and invasion (P < .05) while HULC overexpression led to the opposite results in GEN-treated cells. The expression of phosphatidylinositol 3' -kinase (PI3K)/ protein kinase B (AKT) and c-Jun N-terminal kinase (JNK) was down-regulated by GEN (all P < .05) while reversed by HULC overexpression. HULC was up-regulated in GC. GEN inhibited MNK45 cell viability, colony formation, migration and invasion while induced cell apoptosis by down-regulation of HULC in MKN45 cells. GEN inactivated PI3K/AKT and JNK signal pathways through down-regulation of HULC.