Compound of BMSC, muscle-like cells, and calcium alginate composite gel has the potential to differentiate into muscle cells in the microenvironment of SUI rat model. It is found by LPP measurement that the correlation between the increase in urethral resistance and the volume effect of calcium alginate gel is high.

Abstract. The present study aimed to investigate the role of microRNA-96 (miR-96) in the proliferation, invasion and apoptosis of bladder cancer cell lines, and the associated mechanisms. The expression of miR-96 and human ether-à-go-go-related (HERG1) potassium channel in the normal uroepithelium SV-HUC-1 cell line, and bladder cancer T24 and 5637 cell lines were examined using reverse transcription-polymerase chain reaction or/and western blotting. Transfection with miR-96 inhibitor or scrambled control (SC) was used to study the biological activities of miR-96 in bladder cancer cell lines. MTT, flow cytometric and Transwell assays were applied to detect cell viability, apoptosis and invasion, respectively. A dual-luciferase reporter assay was applied to determine the association between miR-96 and HERG1 expression. As demonstrated, miR-96 was highly expressed in the two bladder cancer cell lines, particularly in T24 cells. Following transfection with miR-96 inhibitor, miR-96 expression was significantly reduced in the T24 cell line, compared with SC. The miR-96 inhibitor suppressed cell proliferation and invasion, promoted apoptosis and arrested the cell cycle at the G 1 phase. Consistently, HERG1 was also highly expressed in the two bladder cancer cell lines at the mRNA and protein level, but not in the normal uroepithelium cell line. The miR-96 inhibitor also significantly decreased HERG1 expression compared with SC. The results of the dual-luciferase reporter assay indicated that miR-96 directly targeted wild-type HERG1. In conclusion, miR-96 inhibitor exhibited anticancer effects on bladder cancer cells by inhibiting proliferation and invasion of cells, and promoting their apoptosis. HERG1 was an important target of miR-96. These results provided experimental evidence supporting miR-96 as a therapeutic target for patients with bladder cancer.

Neural stem cells (NSCs) are a class of self-renewing and undifferentiated progenitor cells that retain the ability to differentiate to neurons, astrocytes and oligodendrocytes. MicroRNAs (miRNAs) are small noncoding RNAs that serve crucial roles in regulating a number of cellular processes, including cell proliferation, differentiation and apoptosis. Our previous GeneChip data indicated that the expression of miR-329-3p was increased in neurons compared with NSCs. However, whether miRNA-329-3p participates in regulating NSC function remains to be elucidated. In the present study, it was identified that the expression of miR-329-3p was upregulated in NSCs during neuronal differentiation, whereas expression of transcription factor E2F1 (E2F1), a putative target gene of miR-329-3p, was downregulated. Using luciferase reporter assays, it was confirmed that miR-329-3p regulated E2F1 expression. As differentiation has been demonstrated to limit the proliferative capacity of NSCs, the effects of miR-329-3p and E2F1 modulation on NSC proliferation were examined. Forced overexpression of miR-329-3p or RNA-mediated silencing of E2F1 inhibited NSC proliferation, and overexpression of miR-329-3p also inhibited E2F1 expression. Notably, ectopic expression of E2F1 reversed the inhibition of NSC proliferation induced by miR-329-3p overexpression. These results indicated that miR-329-3p may serve crucial roles in regulating the proliferation of NSCs, at least in part via inhibition of E2F1 expression. These data improve the understanding of the microRNA-mRNA regulatory network that controls NSC proliferation.

Purpose: To explore the sensitivity of the immunosuppressive agent fingolimod (FTY720) in chordoma and determine whether it can serve as an appropriate alternate treatment for unresectable tumours in patients after incomplete surgery. Methods: Cell viability assays, colony formation assays and EdU assays were performed to evaluate the sensitivity of chordoma cell lines to FTY720. Transwell invasion assays, wound healing assays, flow cytometry, cell cycle analysis, immunofluorescence analysis, Western blotting analysis and enzyme-linked immunosorbent assays (ELISAs) were performed to evaluate cell invasion, epithelial–mesenchymal transition (EMT) and activation of related pathways after treatment with FTY720. The effect of FTY720 was also evaluated in vivo in a xenograft model. Results: We found that FTY720 inhibited the proliferation, invasion and metastasis of sacral chordoma cells (P < 0.01). FTY720 also inhibited the proliferation of tumour cells in a xenograft model using sacral chordoma cell lines (P < 0.01). The mechanism was related to the EMT and apoptosis of chordoma cells and inactivation of IL-6/STAT3 signalling in vitro and in vivo. Conclusions: Our findings indicate that FTY720 may be an effective therapeutic agent against chordoma. These findings suggest that FTY720 is a novel agent that can treat locally advanced and metastatic chordoma.