scholarly journals Downregulation of LAPTM5 suppresses cell proliferation and viability inducing cell cycle arrest at G0/G1 phase of bladder cancer cells

2016 ◽  
Vol 50 (1) ◽  
pp. 263-271 ◽  
Author(s):  
Liang Chen ◽  
Gang Wang ◽  
Yi Luo ◽  
Yongzhi Wang ◽  
Conghua Xie ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
G1 Phase ◽  
Cycle Arrest ◽  
Bladder Cancer Cells

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.

Induction of G1 cell cycle arrest and apoptosis by berberine in bladder cancer cells

2011 ◽  
Vol 661 (1-3) ◽  
pp. 1-7 ◽  
Author(s):  
Keqiang Yan ◽  
Cheng Zhang ◽  
Jinbo Feng ◽  
Lifang Hou ◽  
Lei Yan ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Bladder Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Cycle Arrest ◽  
Bladder Cancer Cells ◽  
G1 Cell Cycle Arrest

Effect of Yes Associated Protein 1 Silence on Proliferation and Apoptosis of Bladder Cancer Cells

2021 ◽  
Vol 11 (5) ◽  
pp. 857-863
Author(s):  
Gaoliang Wu ◽  
Chao Hao ◽  
Xueliang Qi ◽  
Jianqiang Nie
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Direct Role ◽  
Cycle Arrest ◽  
Proliferation And Apoptosis ◽  
Bladder Cancer Cells ◽  
Cancer Tissues

Yes Associated Protein 1 (YAP) can act as either an oncoprotein or a tumor suppressor in different cellular contexts. However, the reports about the direct role of YAP silence in bladder cancer cells are rare. We designed loss-off-function experiments to investigate the effect of YAP knockdown on bladder cancer cell proliferation, cell cycle and cell apoptosis. We examined YAP expression in human bladder cancer and paracancerous tissues using RT-qPCR, western blot and immunohisto-chemistry. YAP short hairpin RNA (shRNA) was successfully constructed and transfected into T24 cells to knockdown YAP. Cell proliferation, cell cycle and cell apoptosis were analyzed by CCK-8 and flow cytometry. We found the expression levels of YAP mRNA and protein were significantly increased in the bladder cancer tissues when compared with that in the paracancerous tissues. shRNA YAP inhibited cell proliferation, induced cell cycle arrest at G1 phase, and induced cell apoptosis. In conclusion, our findings provided the first evidence that YAP knockdown could inhibit cell proliferation and induce cell apoptosis of bladder cancer cells. YAP inhibition may be beneficial in the treatment of bladder cancer.

scholarly journals Knockdown of long non-coding RNA linc00511 suppresses proliferation and promotes apoptosis of bladder cancer cells via suppressing Wnt/β-catenin signaling pathway

2018 ◽  
Vol 38 (4) ◽  
Author(s):  
Jun Li ◽  
Yan Li ◽  
Fandong Meng ◽  
Liye Fu ◽  
Chuize Kong
Keyword(s):  
Cell Cycle ◽  
Bladder Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Noncoding Rna ◽  
Migration And Invasion ◽  
Cycle Arrest ◽  
Bladder Cancer Cells ◽  
Cancer Tissues

More and more studies have shown that long non-coding RNAs (lncRNAs) play critical roles in various biological processes of bladder cancer, including proliferation, apoptosis, migration and cell cycle arrest. LncRNA long intergenic noncoding RNA 00511 (linc00511) is one of the lncRNAs highly expressed in bladder cancer tissues and cells. However, little is known about the roles and mechanisms of linc00511 in bladder cancer. Here, we demonstrated that linc00511 was highly expressed in bladder cancer tissues and cells. Linc00511 knockdown could cause the cell proliferation suppression and cell cycle arrest, which were mediated by p18, p21, CDK4, cyclin D1 and phosphorylation Rb. Suppressed linc00511 could induce the apoptosis in T24 and BIU87 cells via activating the caspase pathway. Down-regulation of linc00511 could also suppress the migration and invasion of T24 and BIU87 cells. In addition, we found that the expression of linc00511 was negatively correlated with that of miR-15a-3p in the clinical bladder cancer samples. Further mechanistic studies showed that linc00511 knockdown induced proliferation inhibition, and apoptosis increase might be regulated through suppressing the activities of Wnt/β-catenin signaling pathway. Thus, we revealed that knockdown of linc00511 suppressed the proliferation and promoted apoptosis of bladder cancer cells through suppressing the activities of Wnt/β-catenin signaling pathway. Moreover, we suggested that linc00511 could be a potential therapeutic target and novel biomarker in bladder cancer.

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