Downregulation of long non-coding RNA UCA1 is associated with the anticancer effects of isorhapontigenin on human bladder cancer cells

Isorhapontigenin (ISO), the dominant active compound of the Chinese herb Gnetum cleistostachyum, has been shown for hundreds of years to exhibit several significant anti-cancer activities, and could possibly inhibit the proliferation of bladder cancer cells. However, details regarding the mechanism of its action are not well defined, especially regarding its regulation of the long non-coding RNA (lncRNA) of urothelial carcinoma antigen 1 (UCA1). To address this issue, human bladder cancer cell strain 5637 was chosen, and cell proliferation activity was assayed with a gradient of ISO for different treatment durations to screen for the optimal treatment concentration and duration. Subsequently, the mRNA expression level of UCA1 was assayed by real-time quantitative polymerase chain reaction (RT-qPCR), cell cycle was assayed by flow cytometry, cell migration activity was assayed by a cell wound healing test, and matrix metalloproteinase (MMP)-2 and MMP-9 expression level was determined by RT-qPCR and western blot analysis. As expected, with increasing concentrations of ISO, the survival rate of 5637 cells was significantly decreased, and treatment with 20 μM ISO for 72 h was validated as an optimal condition. After treatment with 20 μM ISO for 72 h, the mRNA expression level of UCA1 was significantly decreased, the cell cycle was significantly altered with a significant increase in the percentage of cells in G0/G1 phase, and a significant decrease in those in S and G2/M. Moreover, cell migration capacity was significantly decreased, and the mRNA and protein expression levels of MMP-2 and MMP-9 was significantly decreased. These results indicate that ISO could inhibit the proliferation of human bladder cells via downregulation of lncRNA of UCA1, and further downregulation of the cell cycle, cell migration, MMP-2, and MMP-9, not only providing a significant reference for studying the mechanism of human bladder cancer treatment, but also providing potential clinical value.