Identification of several cell cycle relevant genes highly correlated with the progression and prognosis of human bladder urothelial tumor

2019 ◽  
Vol 234 (8) ◽  
pp. 13439-13451 ◽  
Author(s):  
Lu Wang ◽  
Song Chen ◽  
Yongwen Luo ◽  
Lushun Yuan ◽  
Tianchen Peng ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Human Bladder ◽  
Urothelial Tumor ◽  
Highly Correlated

scholarly journals Betulinic Acid Restricts Human Bladder Cancer Cell Proliferation In Vitro by Inducing Caspase-Dependent Cell Death and Cell Cycle Arrest, and Decreasing Metastatic Potential

Molecules ◽  
2021 ◽  
Vol 26 (5) ◽  
pp. 1381
Author(s):  
So Young Kim ◽  
Hyun Hwangbo ◽  
Min Yeong Kim ◽  
Seon Yeong Ji ◽  
Da Hye Kim ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Bladder Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Human Bladder Cancer ◽  
Human Bladder ◽  
Cycle Arrest ◽  
Bladder Cancer Cells ◽  
Induced Apoptosis ◽  
Human Bladder Cancer Cells

Betulinic acid (BA) is a naturally occurring pentacyclic triterpenoid and generally found in the bark of birch trees (Betula sp.). Although several studies have been reported that BA has diverse biological activities, including anti-tumor effects, the underlying anti-cancer mechanism in bladder cancer cells is still lacking. Therefore, this study aims to investigate the anti-proliferative effect of BA in human bladder cancer cell lines T-24, UMUC-3, and 5637, and identify the underlying mechanism. Our results showed that BA induced cell death in bladder cancer cells and that are accompanied by apoptosis, necrosis, and cell cycle arrest. Furthermore, BA decreased the expression of cell cycle regulators, such as cyclin B1, cyclin A, cyclin-dependent kinase (Cdk) 2, cell division cycle (Cdc) 2, and Cdc25c. In addition, BA-induced apoptosis was associated with mitochondrial dysfunction that is caused by loss of mitochondrial membrane potential, which led to the activation of mitochondrial-mediated intrinsic pathway. BA up-regulated the expression of Bcl-2-accociated X protein (Bax) and cleaved poly-ADP ribose polymerase (PARP), and subsequently activated caspase-3, -8, and -9. However, pre-treatment of pan-caspase inhibitor markedly suppressed BA-induced apoptosis. Meanwhile, BA did not affect the levels of intracellular reactive oxygen species (ROS), indicating BA-mediated apoptosis was ROS-independent. Furthermore, we found that BA suppressed the wound healing and invasion ability, and decreased the expression of Snail and Slug in T24 and 5637 cells, and matrix metalloproteinase (MMP)-9 in UMUC-3 cells. Taken together, this is the first study showing that BA suppresses the proliferation of human bladder cancer cells, which is due to induction of apoptosis, necrosis, and cell cycle arrest, and decrease of migration and invasion. Furthermore, BA-induced apoptosis is regulated by caspase-dependent and ROS-independent pathways, and these results provide the underlying anti-proliferative molecular mechanism of BA in human bladder cancer cells.

Characterization of human bladder cancer patient-derived xenograft in vivo and in organoids.

2018 ◽  
Vol 36 (6_suppl) ◽  
pp. 479-479
Author(s):  
Hung-Ming Lam ◽  
Yuzhen Liu ◽  
Funda Vakar-Lopez ◽  
Lisha Brown ◽  
Robert B. Montgomery ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Growth Rate ◽  
Bladder Cancer ◽  
Proliferation Index ◽  
Bladder Cancer Patient ◽  
Human Bladder Cancer ◽  
Human Bladder ◽  
Patient Derived Xenograft ◽  
Late Passage

479 Background: To establish and molecularly characterize a human bladder cancer patient-derived xenograft (PDX) in vivo and in an organoid system derived from the PDX for preclinical studies. Methods: Two-mm3 bits of urothelial carcinoma originated from muscle invasive disease excised in cystectomy were implanted subcutaneously into male severe combined immunodeficient mice to establish PDXs. Established PDXs (CoCaB 1) were passaged subcutaneously in SCID mice and histopathology of each passage was compared with the originating tumor. Tumor size was measured weekly by caliper to determine the growth rate of PDXs from early (P1/P2) through late passage (P8/P9). Representative early and late passages were collected for organoid establishment. For both early and late passages, proliferation was assessed by Ki67 in PDXs and organoids, and cell cycle analysis and MTS assay specifically in organoids. RNA sequencing was performed to compare the fidelity of PDX and organoids vs. primary tumor. Results: Histologically, 16 of the 16 (100%) PDXs generated from early through late passage (1-2 tumors per passage) were similar to the original high-grade urothelial carcinoma. In vivo, the latency of PDX establishment decreased upon passage (9 weeks to take in early P1/2 vs. 2 weeks to take in late P8/9) and the growth rate increased upon passage. Concordantly, Ki67 proliferation index increased from 40% in P1 to 95% in P8 and was positively correlated with increasing passage (Spearman R=0.804, p=0.001). Similarly, in organoids, late passage demonstrated a shorter growth doubling time, higher Ki67 proliferation index, and faster progression through cell cycle. Transcriptional analysis showed that the PDX contained 81-92% human transcripts, whereas organoids contained >99% human transcripts. Conclusions: Bladder cancer PDXs histologically represented the originating disease. PDX and organoid systems demonstrated concordant increase in proliferation upon serial passages, suggesting clonal selection may take place in this aggressive tumor type. Despite more mouse stromal content in PDX, PDX and organoid represent two independent model systems with highly similar biological responses that allow therapeutic studies.

scholarly journals Photothermal exposure of polydopamine-coated branched Au–Ag nanoparticles induces cell cycle arrest, apoptosis, and autophagy in human bladder cancer cells

2018 ◽  
Vol Volume 13 ◽  
pp. 6413-6428 ◽  
Author(s):  
Xiaoming Zhao ◽  
Tianyang Qi ◽  
Chenfei Kong ◽  
Miao Hao ◽  
Yuqian Wang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Bladder Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Ag Nanoparticles ◽  
Human Bladder Cancer ◽  
Human Bladder ◽  
Cycle Arrest ◽  
Bladder Cancer Cells ◽  
Human Bladder Cancer Cells

Cell-Cycle Progression During Continuous Low Dose Rate Irradiation of a Human Bladder Carcinoma Cell Line

1994 ◽  
Vol 19 (1) ◽  
pp. 52
Author(s):  
Krzysztof Skladowski ◽  
Trevor J. McMillan ◽  
John Peacock ◽  
Jennifer Titley ◽  
G. Gordon Steel
Keyword(s):  
Cell Cycle ◽  
Dose Rate ◽  
Bladder Carcinoma ◽  
Cell Cycle Progression ◽  
Low Dose ◽  
Carcinoma Cell ◽  
Human Bladder ◽  
Cycle Progression ◽  
Low Dose Rate ◽  
Bladder Carcinoma Cell Line

Computerized Video Time-Lapse (CVTL) Analysis of Cell Death Kinetics in Human Bladder Carcinoma Cells (EJ30) X-Irradiated in Different Phases of the Cell Cycle

2002 ◽  
Vol 158 (6) ◽  
pp. 667-677 ◽  
Author(s):  
Kenneth Chu ◽  
Edith A. Leonhardt ◽  
Maxine Trinh ◽  
Geraldine Prieur-Carrillo ◽  
Johan Lindqvist ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Bladder Carcinoma ◽  
Time Lapse ◽  
Carcinoma Cells ◽  
Human Bladder ◽  
Death Kinetics ◽  
Bladder Carcinoma Cells

scholarly journals Silencing of mutant p53 by siRNA induces cell cycle arrest and apoptosis in human bladder cancer cells

2013 ◽  
Vol 11 (1) ◽  
pp. 22 ◽  
Author(s):  
Hai-Bin Zhu ◽  
Kai Yang ◽  
Yan-Qi Xie ◽  
Yi-Wei Lin ◽  
Qi-Qi Mao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Bladder Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Mutant P53 ◽  
Human Bladder Cancer ◽  
Human Bladder ◽  
Cycle Arrest ◽  
Bladder Cancer Cells ◽  
Human Bladder Cancer Cells

scholarly journals Changes of Cell Cycle Affecting Cidal Effect of Triethylene Thiophosphoramide on Cultured Human Bladder Carcinoma Cells

1978 ◽  
Vol 125 (2) ◽  
pp. 163-167
Author(s):  
TETSURO KATO ◽  
KIYOSHI ISHIKAWA ◽  
RYOSUKE NEMOTO ◽  
ROBERT J. IRWIN, Jr.
Keyword(s):  
Cell Cycle ◽  
Bladder Carcinoma ◽  
Carcinoma Cells ◽  
Human Bladder ◽  
Bladder Carcinoma Cells
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