scholarly journals Inhibitory effect of Au@Pt-NSs on proliferation, migration, and invasion of EJ bladder carcinoma cells: involvement of cell cycle regulators, signaling pathways, and transcription factor-mediated MMP-9 expression

2018 ◽  
Vol Volume 13 ◽  
pp. 3295-3310 ◽  
Author(s):  
Seung-Shick Shin ◽  
Dae-Hwa Noh ◽  
Byungdoo Hwang ◽  
Jo-Won Lee ◽  
Sung Lyea Park ◽  
...  
Tumor Biology ◽  
2017 ◽  
Vol 39 (2) ◽  
pp. 101042831769167 ◽  
Author(s):  
Ju Guo ◽  
Runfu Cao ◽  
Xingwei Yu ◽  
Zewen Xiao ◽  
Zhiwen Chen

The regulation of initiation and progression during carcinogenesis of bladder carcinoma is not completely elucidated. Dysregulation of microRNAs has been detected to play critical roles in the development of various cancers, including bladder carcinoma, whereas the involvement of miR-223-3p in the tumorigenesis of bladder carcinoma has not been studied. Here, we show that significantly higher levels of nuclear receptor coactivator 1 and significantly lower levels of miR-223-3p were detected in bladder carcinoma tissue, compared to the adjacent non-tumor tissue. In addition, the levels of nuclear receptor coactivator 1 and miR-223-3p were inversely correlated. Moreover, low miR-223-3p levels in bladder carcinoma specimens were associated with poor prognosis. In vitro, depletion of miR-223-3p increased bladder carcinoma cell invasion, which was abolished by overexpression of nuclear receptor coactivator 1. Bioinformatics studies demonstrate that miR-223-3p may bind to the 3′-UTR of nuclear receptor coactivator 1 messenger RNA to inhibit its protein translation in bladder carcinoma cells. Together, our study highlights miR-223-3p as a previously unrecognized microRNA that inhibits bladder carcinoma invasiveness via nuclear receptor coactivator 1, and this finding may be important for developing innovative therapeutic targets in treating bladder carcinoma.


2002 ◽  
Vol 158 (6) ◽  
pp. 667-677 ◽  
Author(s):  
Kenneth Chu ◽  
Edith A. Leonhardt ◽  
Maxine Trinh ◽  
Geraldine Prieur-Carrillo ◽  
Johan Lindqvist ◽  
...  

2016 ◽  
Vol 36 (2) ◽  
pp. 977-983 ◽  
Author(s):  
Naiwen Zhang ◽  
Xiaojun Bi ◽  
Yu Zeng ◽  
Yuyan Zhu ◽  
Zhe Zhang ◽  
...  

Cell Cycle ◽  
2016 ◽  
Vol 15 (15) ◽  
pp. 2042-2052 ◽  
Author(s):  
Karolin Léger ◽  
Ann-Katrin Hopp ◽  
Monika Fey ◽  
Michael O. Hottiger

2019 ◽  
Vol 38 (4) ◽  
pp. 1020-1030 ◽  
Author(s):  
Mariana S. Sonego ◽  
Natália V. Segatto ◽  
Lucas Damé ◽  
Mariana Fronza ◽  
Carolina B. Gomes ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Ke-Hung Tsui ◽  
Shyi-Wu Wang ◽  
Li-Chuan Chung ◽  
Tsui-Hsia Feng ◽  
Tzu-Yi Lee ◽  
...  

Interleukin-6, a multifunctional cytokine, contributes to tumor cell proliferation and differentiation. However, the biological mechanisms that are affected by the expression of interleukin-6 in bladder cancer cells remain unclear. We evaluated the effects of interleukin-6 expression in human bladder carcinoma cellsin vitroandin vivo. The results of interleukin-6-knockdown experiments in T24 cells and interleukin-6-overexpression experiments in HT1376 cells revealed that interleukin-6 reduced cell proliferation, migration, and invasionin vitro. Xenograft animal studies indicated that the overexpression of interleukin-6 downregulated tumorigenesis of bladder cells and that interleukin-6 knockdown reversed this effect. The results of RT-PCR, immunoblotting, and reporter assays indicated that the overexpression of interleukin-6 upregulated the expression of the mammary serine protease inhibitor (MASPIN), N-myc downstream gene 1 (NDRG1), and KAI1 proteins in HT1376 cells and that interleukin-6 knockdown reduced the expression of these proteins in T24 cells. In addition, results of immunoblotting assays revealed that interleukin-6 modulated epithelial-mesenchymal transitions by upregulating the expression of the E-cadherin, while downregulation N-cadherin and vimentin proteins. Our results suggest that the effects of interleukin-6 on the regulation of epithelial-mesenchymal transitions and the expressions of the MASPIN, NDRG1, and KAI1 genes attribute to the modulation of tumorigenesis in human bladder carcinoma cells.


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