ANTI-INVASION AND ANTI-METASTASIS EFFECTS OF DANDELION (TARAXACUM OFFICINALE) HYDROALCOHOLIC EXTRACT ON GLIOBLASTOMA MULTIFORME CELL LINE MODEL

Objective: Glioblastoma multiforme is one of the malignant brain tumors and despite recent advancements in cancer treatment remains largely incurable. Cancer invasion has a cascade of interrelated and sequential steps, including cell adhesion, extracellular matrix degradation, and cell movement. Hence, inhibition of the invasion-associated steps could be a potential strategy for prolonging the life of patients. This study aimed to evaluate the anti-invasion and anti-metastasis effects of Dandelion (Taraxacum officinale) hydro-alcoholic extract on glioblastoma multiforme cell line (U87MG). Materials and Methods: The hydro-alcoholic extract was prepared, and the cell line was treated with 1000, 500, 250, 125, and 62.5 mu g / ml of extract for 24, 48, and 72 hr. Cell viability was evaluated. The effect of extract (IC50 concentration) on cancer cell invasion potential was tested. The expression levels of MMP-2, MMP-9, TIMP-1, TIMP-2, uPA, uPAR, p38MAPK, ERK1/2, and SAPK/JNK were analyzed. Comparisons between groups were performed by Tukey's test one-way analysis of variance and differences were considered significant when p<0.05. Results: After treatment with extract, the cells viability was decrease in a concentration- and time-dependent. IC50 concentration of dandelion extract significantly decreased the cell migration by 32% (p<0.05), cell invasion potential by 77% (p<0.05) and cell adhesion by 51% (p<0.05). Also, the expression levels of proteolytic enzymes associated with matrix and base membrane degradation (MMP-2, MMP-9, and uPA) were decreased and the levels of their endogenous inhibitors (TIMP1 and TIMP2) were increased. Moreover, the p38MAPK and SAPK/JNK signaling pathway, which stimulates proteolytic enzymes and matrix degradation, was inhibited by extract treatment. Conclusions: Dandelion extract reduced the viability and invasion potential of the glioblastoma cells by regulating proteolytic enzymes and matrix dynamics through the p38MAPK and SAPK/JNK pathway.