Induction of drug-resistant bladder carcinoma cells in vitro: impact on polychemotherapy with cisplatin, methotrexate and vinblastine (CMV)

1998 ◽  
Vol 26 (4) ◽  
pp. 249-257 ◽  
Author(s):  
Detlef Rohde ◽  
Bernhard Brehmer ◽  
Tanja Kapp ◽  
Markus Valdor ◽  
Gerhard Jakse
Keyword(s):  
Bladder Carcinoma ◽  
Carcinoma Cells ◽  
Drug Resistant ◽  
Bladder Carcinoma Cells

scholarly journals Transgelin, a p53 and PTEN-Upregulated Gene, Inhibits the Cell Proliferation and Invasion of Human Bladder Carcinoma Cells in Vitro and in Vivo

2019 ◽  
Vol 20 (19) ◽  
pp. 4946 ◽  
Author(s):  
Tsui ◽  
Lin ◽  
Chang ◽  
Hou ◽  
Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cells ◽  
Bladder Carcinoma ◽  
Carcinoma Cells ◽  
Human Bladder ◽  
Ectopic Overexpression ◽  
Proliferation And Invasion ◽  
Bladder Carcinoma Cells

Transgelin (TAGLN/SM22-α) is a regulator of the actin cytoskeleton, affecting the survival, migration, and apoptosis of various cancer cells divergently; however, the roles of TAGLN in bladder carcinoma cells remain inconclusive. We compared expressions of TAGLN in human bladder carcinoma cells to the normal human bladder tissues to determine the potential biological functions and regulatory mechanisms of TAGLN in bladder carcinoma cells. Results of RT-qPCR and immunoblot assays indicated that TAGLN expressions were higher in bladder smooth muscle cells, fibroblast cells, and normal epithelial cells than in carcinoma cells (RT-4, HT1376, TSGH-8301, and T24) in vitro. Besides, the results of RT-qPCR revealed that TAGLN expressions were higher in normal tissues than the paired tumor tissues. In vitro, TAGLN knockdown enhanced cell proliferation and invasion, while overexpression of TAGLN had the inverse effects in bladder carcinoma cells. Meanwhile, ectopic overexpression of TAGLN attenuated tumorigenesis in vivo. Immunofluorescence and immunoblot assays showed that TAGLN was predominantly in the cytosol and colocalized with F-actin. Ectopic overexpression of either p53 or PTEN induced TAGLN expression, while p53 knockdown downregulated TAGLN expression in bladder carcinoma cells. Our results indicate that TAGLN is a p53 and PTEN-upregulated gene, expressing higher levels in normal bladder epithelial cells than carcinoma cells. Further, TAGLN inhibited cell proliferation and invasion in vitro and blocked tumorigenesis in vivo. Collectively, it can be concluded that TAGLN is an antitumor gene in the human bladder.

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 Metallothionein 3 Is a Hypoxia-Upregulated Oncogene Enhancing Cell Invasion and Tumorigenesis in Human Bladder Carcinoma Cells

2019 ◽  
Vol 20 (4) ◽  
pp. 980 ◽  
Author(s):  
Ke-Hung Tsui ◽  
Chen-Pang Hou ◽  
Kang-Shuo Chang ◽  
Yu-Hsiang Lin ◽  
Tsui-Hsia Feng ◽  
...  
Keyword(s):  
Bladder Carcinoma ◽  
Annexin V ◽  
Carcinoma Cells ◽  
Gene Expressions ◽  
T24 Cells ◽  
Apoptosis Assay ◽  
Induced Apoptosis ◽  
Bladder Carcinoma Cells

Metallothioneins have been viewed as modulators in a number of biological regulations regarding cancerous development; however, the function of metallothionein 3 (MT3) in bladder cancer is unexplored. We determined the regulatory mechanisms and potential function of MT3 in bladder carcinoma cells. Real-Time Reverse Transcriptase-Polymerase Chain Reaction (RT-qPCR) assays revealed that TSGH-8301 cells expressed more MT3 levels than RT-4, HT1376, and T24 cells. Immunoblot and RT-qPCR assays showed that arsenic (AS2O3) treatments enhanced the gene expression of MT3. Hypoxia induced HIF-1α, HIF-2α, and MT3 expression; furthermore, HIF-2α-knockdown attenuated hypoxic activation on MT3 expression. Ectopic overexpression of MT3 increased cell proliferation, invasion, and tumorigenesis significantly in T24 and HT1376 cells in vitro and in vivo; however, MT3-knockdown in TSGH-8301 cells had the reverse effect. Moreover, knockdown of MT3 enhanced arsenic-induced apoptosis determined by the Annexin V-FITC apoptosis assay. MT3-overexpression downregulated the gene expressions of N-myc downstream regulated gene 1 (NDRG1), N-myc downstream regulated gene 2 (NDRG2), and the mammary serine protease inhibitor (MASPIN) in HT1376 and T24 cells, whereas MT3-knockdown in TSGH-8301 cells had the opposite effect. The experiments indicated that MT3 is an arsenic- and hypoxia-upregulated oncogene that promotes cell growth and invasion of bladder carcinoma cells via downregulation of NDRG1, NDRG2, and MASPIN expressions.

The src-family kinase inhibitor PP2 suppresses the in vitro invasive phenotype of bladder carcinoma cells via modulation of Akt

2005 ◽  
Vol 96 (3) ◽  
pp. 416-422 ◽  
Author(s):  
George J. Chiang ◽  
Brian R. Billmeyer ◽  
David Canes ◽  
John Stoffel ◽  
Alireza Moinzadeh ◽  
...  
Keyword(s):  
Bladder Carcinoma ◽  
Kinase Inhibitor ◽  
Carcinoma Cells ◽  
Src Family Kinase ◽  
Invasive Phenotype ◽  
Bladder Carcinoma Cells
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