scholarly journals FGFR inhibitor BGJ398 and HDAC inhibitor OBP-801 synergistically inhibit cell growth and induce apoptosis in bladder cancer cells

2017 ◽  
Author(s):  
Toshiya Takamura ◽  
Mano Horinaka ◽  
Shusuke Yasuda ◽  
Seijiro Toriyama ◽  
Yuichi Aono ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Hdac Inhibitor ◽  
Bladder Cancer Cells ◽  
Inhibit Cell Growth

Ailanthone inhibits cell growth and migration of cisplatin resistant bladder cancer cells through down-regulation of Nrf2, YAP, and c-Myc expression.

Phytomedicine ◽  
2019 ◽  
Vol 56 ◽  
pp. 156-164 ◽  
Author(s):  
Martina Daga ◽  
Stefania Pizzimenti ◽  
Chiara Dianzani ◽  
Marie Angele Cucci ◽  
Roberta Cavalli ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Down Regulation ◽  
Cell Growth And Migration ◽  
Bladder Cancer Cells ◽  
And Migration

scholarly journals The Antitumor Effect of Curcumin in Urothelial Cancer Cells Is Enhanced by Light Exposure In Vitro

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Frederik Roos ◽  
Katherina Binder ◽  
Jochen Rutz ◽  
Sebastian Maxeiner ◽  
August Bernd ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cell Growth ◽  
Visible Light ◽  
Cancer Cells ◽  
Cell Lines ◽  
Light Exposure ◽  
Bladder Cancer Cells

The natural compound curcumin exerts antitumor properties in vitro, but its clinical application is limited due to low bioavailability. Light exposure in skin and skin cancer cells has been shown to improve curcumin bioavailability; thus, the object of this investigation was to determine whether light exposure might also enhance curcumin efficacy in bladder cancer cell lines. RT112, UMUC3, and TCCSUP cells were preincubated with low curcumin concentrations (0.1-0.4μg/ml) and then exposed to 1.65 J/cm2visible light for 5 min. Cell growth, cell proliferation, apoptosis, cell cycle progression, and cell cycle regulating proteins along with acetylation of histone H3 and H4 were investigated. Though curcumin alone did not alter cell proliferation or apoptosis, tumor cell growth and proliferation were strongly blocked when curcumin was combined with visible light. Curcumin-light caused the bladder cancer cells to become arrested in different cell phases: G0/G1 for RT112, G2/M for TCCSUP, and G2/M- and S-phase for UMUC3. Proteins of the Cdk-cyclin axis were diminished in RT112 after application of 0.1 and 0.4μg/ml curcumin. Cell cycling proteins were upregulated in TCCSUP and UMUC3 in the presence of 0.1μg/ml curcumin-light but were partially downregulated with 0.4μg/ml curcumin. 0.4μg/ml (but not 0.1μg/ml) curcumin-light also evoked late apoptosis in TCCSUP and UMUC3 cells. H3 and H4 acetylation was found in UMUC3 cells treated with 0.4μg/ml curcumin alone or with 0.1μg/ml curcumin-light, pointing to an epigenetic mechanism. Light exposure enhanced the antitumor potential of curcumin on bladder cancer cells but by different molecular action modes in the different cell lines. Further studies are necessary to evaluate whether intravesical curcumin application, combined with visible light, might become an innovative tool in combating bladder cancer.

scholarly journals Chronic Sulforaphane Administration Inhibits Resistance to the mTOR-Inhibitor Everolimus in Bladder Cancer Cells

2020 ◽  
Vol 21 (11) ◽  
pp. 4026 ◽  
Author(s):  
Saira Justin ◽  
Jochen Rutz ◽  
Sebastian Maxeiner ◽  
Felix K.-H. Chun ◽  
Eva Juengel ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Bladder Cancer ◽  
Cell Growth ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Mtor Inhibitor ◽  
Down Regulation ◽  
Resistance Development ◽  
Bladder Cancer Cells

Progressive bladder cancer growth is associated with abnormal activation of the mammalian target of the rapamycin (mTOR) pathway, but treatment with an mTOR inhibitor has not been as effective as expected. Rather, resistance develops under chronic drug use, prompting many patients to lower their relapse risk by turning to natural, plant-derived products. The present study was designed to evaluate whether the natural compound, sulforaphane (SFN), combined with the mTOR inhibitor everolimus, could block the growth and proliferation of bladder cancer cells in the short- and long-term. The bladder cancer cell lines RT112, UMUC3, and TCCSUP were exposed short- (24 h) or long-term (8 weeks) to everolimus (0.5 nM) or SFN (2.5 µM) alone or in combination. Cell growth, proliferation, apoptosis, cell cycle progression, and cell cycle regulating proteins were evaluated. siRNA blockade was used to investigate the functional impact of the proteins. Short-term application of SFN and/or everolimus resulted in significant tumor growth suppression, with additive inhibition on clonogenic tumor growth. Long-term everolimus treatment resulted in resistance development characterized by continued growth, and was associated with elevated Akt-mTOR signaling and cyclin-dependent kinase (CDK)1 phosphorylation and down-regulation of p19 and p27. In contrast, SFN alone or SFN+everolimus reduced cell growth and proliferation. Akt and Rictor signaling remained low, and p19 and p27 expressions were high under combined drug treatment. Long-term exposure to SFN+everolimus also induced acetylation of the H3 and H4 histones. Phosphorylation of CDK1 was diminished, whereby down-regulation of CDK1 and its binding partner, Cyclin B, inhibited tumor growth. In conclusion, the addition of SFN to the long-term everolimus application inhibits resistance development in bladder cancer cells in vitro. Therefore, sulforaphane may hold potential for treating bladder carcinoma in patients with resistance to an mTOR inhibitor.

scholarly journals Inhibition of NEDD4 inhibits cell growth and invasion and induces cell apoptosis in bladder cancer cells

Cell Cycle ◽  
2017 ◽  
Vol 16 (16) ◽  
pp. 1509-1514 ◽  
Author(s):  
Wu Wen ◽  
Jingying Li ◽  
Longwang Wang ◽  
Yifei Xing ◽  
Xuechao Li ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Bladder Cancer Cells

scholarly journals MMAC1/PTEN inhibits cell growth and induces chemosensitivity to doxorubicin in human bladder cancer cells

Oncogene ◽  
2000 ◽  
Vol 19 (47) ◽  
pp. 5406-5412 ◽  
Author(s):  
Motoyoshi Tanaka ◽  
Dimpy Koul ◽  
Michael A Davies ◽  
Monica Liebert ◽  
Peter A Steck ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Human Bladder Cancer ◽  
Human Bladder ◽  
Bladder Cancer Cells ◽  
Human Bladder Cancer Cells

scholarly journals Pharmacological Inhibition of miR-130 Family Suppresses Bladder Tumor Growth by Targeting Various Oncogenic Pathways via PTPN1

2021 ◽  
Vol 22 (9) ◽  
pp. 4751
Author(s):  
Yuya Monoe ◽  
Kentaro Jingushi ◽  
Akitaka Kawase ◽  
Takayuki Hirono ◽  
Ryo Hirose ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Nucleic Acid ◽  
Cell Growth ◽  
Cancer Cells ◽  
Fiber Formation ◽  
Negative Regulator ◽  
Locked Nucleic Acid ◽  
Luciferase Assay ◽  
Pharmacological Inhibition ◽  
Bladder Cancer Cells

Previously, we have revealed that the miR-130 family (miR-130b, miR-301a, and miR-301b) functions as an oncomiR in bladder cancer. The pharmacological inhibition of the miR-130 family molecules by the seed-targeting strategy with an 8-mer tiny locked nucleic acid (LNA) inhibits the growth, migration, and invasion of bladder cancer cells by repressing stress fiber formation. Here, we searched for a functionally advanced target sequence with LNA for the miR-130 family with low cytotoxicity and found LNA #9 (A(L)^i^i^A(L)^T(L)^T(L)^G(L)^5(L)^A(L)^5(L)^T(L)^G) as a candidate LNA. LNA #9 inhibited cell growth in vitro and in an in vivo orthotopic bladder cancer model. Proteome-wide tyrosine phosphorylation analysis suggested that the miR-130 family upregulates a wide range of receptor tyrosine kinases (RTKs) signaling via the expression of phosphorylated Src (pSrcTyr416). SILAC-based proteome analysis and a luciferase assay identified protein tyrosine phosphatase non-receptor type 1 (PTPN1), which is implicated as a negative regulator of multiple signaling pathways downstream of RTKs as a target gene of the miR-130 family. The miR-130-targeted LNA increased and decreased PTPN1 and pSrcTyr416 expressions, respectively. PTPN1 knockdown led to increased tumor properties (cell growth, invasion, and migration) and increased pSrcTyr416 expression in bladder cancer cells, suggesting that the miR-130 family upregulates multiple RTK signaling by targeting PTPN1 and subsequent Src activation in bladder cancer. Thus, our newly designed miR-130 family targeting LNA could be a promising nucleic acid therapeutic agent for bladder cancer.

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