Effect of Licochalcone-A Combined with Gene on Proliferation of Glioma U251 Cells.

This research aimed to explore the effect of Licochalcone-A (LCA) combined with gene on the proliferation, migration, and invasion of glioma U251 cells through the Wnt/-catenin signaling pathway. The glioma U251 cell line was taken as the research object, and the Rab23 overexpression plasmid was constructed. According to the treatment method, U251 cells were rolled into blank control group (BC), Rab23 overexpression plasmid transfection group (Rab23), 25 mol·L LCA treatment group (LCA), and Rab23 overexpression plasmid transfection combined with 25 mol·L LCA treatment group (Rab23 + LCA). Subsequently, the ability of cell proliferation, migration, and invasion of each group was detected by methyl thiazolyl tetrazolium (MTT) assay, scratch healing test, and Transwell cell invasion test, respectively. Western blot was implemented to detect the expression differences of cell proliferation antigen Ki-67, apoptosis-related proteins Bcl-2 and Bax, and Wnt/-catenin pathway-related proteins -catenin, glycogen synthase kinase-3 (GSK3), Axin2, and c-myc. The results showed the successful construction of Rab23 overexpression and stable transfection U251 cell line. After grouping and treatments, the cell proliferation, migration, and invasion ability of the Rab23 group, LCA group, and Rab23 + LCA group was substantially reduced relative to BC group ( < 0.05). In addition, the cell proliferation, migration, and invasion ability of Rab23 + LCA group decreased relatively more significantly. The expression levels of Ki-67, Bcl-2, -catenin, and c-myc in the Rab23, LCA, and Rab23 + LCA groups were greatly lower versus those of BC group. Moreover, the protein expression levels of Bax, GSK3, and Axin2 were considerably increased ( < 0.05), while the expression of protein in Rab23 + LCA group increased notably. These findings indicate that LCA combined with gene can inhibit the proliferation, migration, and invasion of glioma U251 cells through the Wnt/-catenin signaling and can promote cell apoptosis.