High Expression of Vimentin is Associated With Progression and a Poor Outcome in Glioblastoma.

Glioblastoma multiforme (GBM) has a high recurrence and mortality rate. Because of a poor understanding of the mechanism for this disease, treatment regimens have remained limited. Vimentin, one of the major cytoskeletal proteins, is associated with cellular structure. However, the function of vimentin in GBM is still undefined. In the present study, we investigated the expression level of vimentin in 179 GBM tissues using immunohistochemistry. We found that the vimentin expression level was associated with the time to progression (P=0.029). A Kaplan-Meier analysis revealed that patients with high vimentin expression had a significantly shorter overall survival (P=0.0002) and progression-free survival (P=0.0001) compared with those with low expression. Furthermore, in vitro experiments showed that withaferin-A, a chemical inhibitor of vimentin, could inhibit GBM cell migration and invasion activity when its concentrations were <0.5 µM, and higher concentrations of withaferin-A could decrease the viability of U251and U87 cells significantly. In conclusion, our results indicated that vimentin may play an important role in the progression of GBM.

Downregulation of miR-21 is involved in direct actions of ursolic acid on the heart: implications for cardiac fibrosis and hypertrophy.

PURPOSE: Myocardial fibrosis contributes to cardiac remodeling and loss of cardiac function in myocardial infarction and heart failure. This study used in vitro and in vivo models to examine the effects of ursolic acid (UA) on myocardial fibrosis and to explore its potential mechanism. METHODS: Transverse aortic constriction (TAC) surgery was performed in mice to induce cardiac hypertrophy and fibrosis. UA was orally administered 1 week prior to TAC. Two weeks after TAC, myocardial pathology was detected using Masson's trichrome staining and transmission electron microscopy, and heart-to-body weight ratio was measured. For in vitro studies, cultured cardiac fibroblasts were treated with serum in the presence or absence of UA. The relative levels of miR-21 and p-ERK/ERK, collagen content and cell viability were measured. RESULTS: Ursolic acid attenuated pathological cardiac hypertrophy and myocardial fibrosis in vivo induced by TAC. Downregulation of miR-21 and p-ERK/ERK were observed in myocardial fibroblasts treated with UA in a dose-dependent manner compared with the control group both in vitro and in vivo. CONCLUSIONS: Our study demonstrates that UA can inhibit myocardial fibrosis both in vitro and in vivo, and the effects of UA on myocardial fibrosis may be due to the inhibition of miR-21/ERK signaling pathways.