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Wang Y.-B.,Nanchang University | Fu B.,Nanchang University | Fu B.,Jiangxi Institute of Urology | Wang G.-X.,Nanchang University | And 7 more authors.
Tumor | Year: 2014

Objective: To investigate the effects of inhibition of microRNA-221 (miR-221) expression on the proliferation and apoptosis of bladder cancer cells. Methods: Has-miR-221 inhibitor and has-miR-221 inhibitor negative control were synthesized, and then transfected into bladder cancer T24 and J82 cells. The transfection efficiency was observed under a fluorescence microscope 5 h after transfection. The expression levels of miR-221 in T24 and J82 cells were detected by real-time fluorescence quantitative PCR at 24, 48 and 72 h after transfection; the proliferation of T24 and J82 cells was also detected by MTT assay. The expression levels of p53 upregulated modulator of apoptosis (PUMA), Bax and Bcl-2 mRNAs and proteins in T24 and J82 cells 48 h after transfection were measured by RT-PCR and Western blotting, respectively; the apoptosis of T24 and J82 cells was determined by flow cytometry (FCM) and acridine orange (AO)-ethidium bromide (EB) staining. Results: The efficiencies of has-miR-221 inhibitor transfection into T24 and J82 cells were 80% and 90%, respectively. The expression levels of miR-221 in T24 and J82 cells after transfection with has-miR-221 inhibitor were lower than those in the negative control group and the blank control group (only adding liposome) (P < 0.05). The proliferative inhibition rates of T24 and J82 cells after transfection with has-miR-221 inhibitor were higher than those in the negative control group and the blank control group (P < 0.05), and this effect was in a time-dependent manner. The expression levels of PUMA and Bax mRNAs and proteins in T24 and J82 cells after transfection with has-miR-221 inhibitor were higher than those in the negative control group and the blank control group (P < 0.05), and the expression levels of Bcl-2 mRNA and protein were opposite (P < 0.05). The apoptosis rates of T24 and J82 cells after transfection with has-miR-221 inhibitor were higher than those in the negative control group and the blank control group (P < 0.05). Conclusion: Inhibition of miR-221 expression can suppress the proliferation of bladder cancer cells and induce apoptosis. Copyright© 2014 by Tumor. Source


Fu B.,Nanchang University | Fu B.,Jiangxi Institute of Urology | Wang Y.,Nanchang University | Zhang X.,Nanchang University | And 9 more authors.
International Journal of Oncology | Year: 2015

Immune evasion of cancer cells is mainly due to the impaired transduction of apoptotic signals from immune cells to cancer cells, as well as inhibition of subsequent apoptosis signal cascades within the cancer cells. Over the past few decades, the research has focused more on the impaired transduction of the apoptotic signal from immune cells to cancer cells, rather than inhibition of the intracellular signaling pathways. In this study, miR-221 inhibitor was transfected into bladder cancer cell lines 5637, J82 and T24 to repress the expression of miR-221. As a result, the repression of miR-221 on p53 upregulated modulator of apoptosis (PUMA) was abolished, resulting in increased expression of the pro-apoptotic Bax and reduced expression of the anti-apoptotic Bcl-2, which promotes apoptosis of bladder cancer cells. The expression of MMP-2, MMP-9 and VEGF-C were reduced, resulting in reduced invasiveness and infiltration capability of bladder cancer cells, thereby inhibiting the immune evasion of bladder cancer cells. Source

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