scholarly journals Bufalin prevents the migration and invasion of T24 bladder carcinoma cells through the inactivation of matrix metalloproteinases and modulation of tight junctions

2012 ◽  
Vol 42 (1) ◽  
pp. 277-286 ◽  
Author(s):  
SU HYUN HONG ◽  
GI-YOUNG KIM ◽  
YOUNG-CHAE CHANG ◽  
SUNG-KWON MOON ◽  
WUN-JAE KIM ◽  
...  
Keyword(s):  
Matrix Metalloproteinases ◽  
Tight Junctions ◽  
Bladder Carcinoma ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Bladder Carcinoma Cells

scholarly journals MicroRNA-223-3p inhibits human bladder cancer cell migration and invasion

Tumor Biology ◽  
2017 ◽  
Vol 39 (2) ◽  
pp. 101042831769167 ◽  
Author(s):  
Ju Guo ◽  
Runfu Cao ◽  
Xingwei Yu ◽  
Zewen Xiao ◽  
Zhiwen Chen
Keyword(s):  
Nuclear Receptor ◽  
Bladder Carcinoma ◽  
Messenger Rna ◽  
Tumor Tissue ◽  
Protein Translation ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Nuclear Receptor Coactivator ◽  
Bladder Carcinoma Cells

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.

scholarly journals TGF-β1 promotes the migration and invasion of bladder carcinoma cells by increasing fascin1 expression

2016 ◽  
Vol 36 (2) ◽  
pp. 977-983 ◽  
Author(s):  
Naiwen Zhang ◽  
Xiaojun Bi ◽  
Yu Zeng ◽  
Yuyan Zhu ◽  
Zhe Zhang ◽  
...  
Keyword(s):  
Bladder Carcinoma ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Tgf Β1 ◽  
Bladder Carcinoma Cells

scholarly journals Mechanisms by Which Interleukin-6 Attenuates Cell Invasion and Tumorigenesis in Human Bladder Carcinoma Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Ke-Hung Tsui ◽  
Shyi-Wu Wang ◽  
Li-Chuan Chung ◽  
Tsui-Hsia Feng ◽  
Tzu-Yi Lee ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Bladder Carcinoma ◽  
Interleukin 6 ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Human Bladder ◽  
T24 Cells ◽  
Bladder Carcinoma Cells

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.

scholarly journals Molecular targets for the protodynamic action of cis-urocanic acid in human bladder carcinoma cells

BMC Cancer ◽  
2010 ◽  
Vol 10 (1) ◽  
Author(s):  
Emilia Peuhu ◽  
Aura Kaunisto ◽  
Jarmo K Laihia ◽  
Lasse Leino ◽  
John E Eriksson
Keyword(s):  
Bladder Carcinoma ◽  
Molecular Targets ◽  
Urocanic Acid ◽  
Carcinoma Cells ◽  
Human Bladder ◽  
Bladder Carcinoma Cells

scholarly journals Characterization of the system L amino acid transporter in T24 human bladder carcinoma cells

2002 ◽  
Vol 1565 (1) ◽  
pp. 112-122 ◽  
Author(s):  
Do Kyung Kim ◽  
Yoshikatsu Kanai ◽  
Hye Won Choi ◽  
Sahatchai Tangtrongsup ◽  
Arthit Chairoungdua ◽  
...  
Keyword(s):  
Amino Acid ◽  
Bladder Carcinoma ◽  
Amino Acid Transporter ◽  
Carcinoma Cells ◽  
Human Bladder ◽  
System L ◽  
Acid Transporter ◽  
Bladder Carcinoma Cells
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