scholarly journals TAZ Regulates Bladder Cancer Cell Proliferation and Apoptosis via p38 Activity

2020 ◽  
Author(s):  
Yangyang Sun ◽  
Lianxin Hu ◽  
Chengxi Liu ◽  
Ganglin Su ◽  
Lina Yang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Western Blot ◽  
Cancer Cells ◽  
P38 Mapk ◽  
Mapk Pathway ◽  
Proliferation Assay ◽  
P38 Inhibitor ◽  
Proliferation And Apoptosis ◽  
Bladder Cancer Cells

Abstract Background The progression of cancer is driven by the deregulation of various signaling pathways, especially Hippo and p38 MAPK pathway. TAZ, a downstream target of Hippo pathway, has been demonstrated to promote tumorigenesis in various cancers, but the functions of both Hippo and p38 signaling in bladder cancer cells are still unclear. Methods T24 and 5637 cells with knockdown of TAZ were constructed. EdU cell proliferation assay and western blot were used to illustrate the effects of TAZ on the proliferation and apoptosis of bladder cancer cells and the expression of p38 protein and phosphorylation. We overexpressed Flag-tagged TAZ in 293T cells. Western blot and RT-qPCR were used to further illustrate the effect of TAZ on the expression level of p38. The p38 inhibitor (PH-797804) combined with western blot and EDU cell proliferation assay were used to show whether TAZ affects the proliferation and apoptosis of bladder cancer cells by regulating the activity of p38.Results The shTAZ contained in T24 and 5637 cells significantly inhibited bladder cancer cells proliferation, in addition, the knockdown of TAZ-induced apoptosis of T24 and 5637 cells was found out. The loss of TAZ led to the upregulation of p38 protein as well as phosphorylation. The over-expression of Flag-TAZ had no obvious effect on p38 mRNA level, but p38 protein was reduced clearly in 293T cells. ShTAZ induced the upregulation of cleaved-caspase 3, which disappeared when treated with PH-797804, a p38 inhibitor, and the reduction to EdU positive cells induced by shTAZ was reversed by PH-797804 treatment, which suggested that p38 activity could mediate both cell proliferation and apoptosis regulated by TAZ knockdown. Conclusions In this study, it was demonstrated that TAZ could regulate the proliferation and apoptosis of bladder cancer cells by regulating the stability of p38 protein. Our finding uncovered the novel functional interaction between Hippo and p38 MAPK pathway. An in-depth understanding of this question may indicate a new direction of diagnosis or treatment for bladder cancer.

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 Down-regulation LncRNA-SNHG15 contributes to proliferation and invasion of bladder cancer cells

BMC Urology ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Aldhabi Mokhtar ◽  
Chuize Kong ◽  
Zhe Zhang ◽  
Yan Du
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Tumor Stage ◽  
Rt Pcr ◽  
Down Regulation ◽  
Bladder Cancer Cells ◽  
Cancer Tissues ◽  
Proliferation And Invasion

Abstract Objectives The aim of this study was to investigate the effect of lncRNA-SNHG15 in bladder carcinoma using cell lines experiments and the relationship between clinical characteristics and lncRNA-SNHG15 expression was analyzed. Methods Bladder cancer tissues and near-cancer tissues were collected. The real-time PCR (RT-PCR) was used to detect the expression of lncRNA-SNHG15 in tissues and cell lines. The expression of lncRNA-SNHG15 was downregulated by interference (siRNA), as detected by RT-PCR, that was used to determine the efficiency of the interference. CCK-8 and Transwell assays were used to evaluate the effect of lncRNA-SNHG15 on the proliferation and invasion capability of bladder cancer cells. The t-test was used for Statistical analyses, which were carried out using the Statistical Graph pad 8.0.1.224 software. Result The expression of lncRNA-SNHG15 was up regulated in 5637, UMUC3 and T24 cell lines compared with corresponding normal controls (P < 0.05). Up regulation was positively related to tumor stage (P = 0.015). And tumor size (P = 0.0465). The down-regulation of lncRNA-SNHG15 with siRNA significantly inhibited UMUC3 and T24 cell proliferation and invasion. Conclusion This study showed that lncRNA-SNHG15 is overexpressed in bladder cancer tissues and (5637, UMUC3 T24) cell lines. Up regulation was positively related to tumor stage (P = 0.015), and tumor size (P = 0.0465). Down-regulation of lncRNA-SNHG15 by siRNA significantly inhibited UMUC3 and T24 cell proliferation and invasion, indicating a potential molecular target for future tumor targeted therapy.

scholarly journals Study of LBHD1 Expression with Invasion and Migration of Bladder Cancer

2019 ◽  
Vol 14 (1) ◽  
pp. 440-447
Author(s):  
Chunhui Dong ◽  
Yihui Liu ◽  
Guiping Yu ◽  
Xu Li ◽  
Ling Chen
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Tumor Antigens ◽  
Urinary Bladder Cancer ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Invasion And Migration ◽  
Bladder Cancer Cells

AbstractLBHD1 (C11ORF48) is one of the ten potential tumor antigens identified by immunoscreening the urinary bladder cancer cDNA library in our previous study. We suspect that its expression is associated with human bladder cancer. However, the exact correlation remains unclear. To address the potential functional relationship between LBHD1 and bladder cancer, we examined the LBHD1 expression at the mRNA and protein level in 5 different bladder cancer cell lines: J82, T24, 253J, 5637, and BLZ-211. LBHD1 high and low expressing cells were used to investigate the migration, invasion, and proliferation of bladder cancer cells following transfection of LBHD1 with siRNA and plasmids, respectively. Our experiment showed that the degree of gene expression was positively related to the migration and invasion of the cancer cells while it had little effect on cell proliferation. Knocking down LBHD1 expression with LBHD1 siRNA significantly attenuated cell migration and invasion in cultured bladder cancer cells, and overexpressing LBHD1 with LBHD1 cDNA plasmids exacerbated cell migration and invasion. Nevertheless, a difference in cell proliferation after transfection of LBHD1 siRNA and LBHD1 cDNA plasmids was not found. Our findings suggest that LBHD1 might play a role in cell migration and invasion.

scholarly journals miR-138-5p contributes to cell proliferation and invasion by targeting Survivin in bladder cancer cells

2016 ◽  
Vol 15 (1) ◽  
Author(s):  
Rong Yang ◽  
Minghui Liu ◽  
Hongwei Liang ◽  
Suhan Guo ◽  
Xu Guo ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cancer Cells ◽  
Bladder Cancer Cells ◽  
Proliferation And Invasion

scholarly journals Polyporus polysaccharide regulates proliferation, apoptosis and migration of bladder cancer cells by polarizing macrophages to M1 subtype in tumor microenvironment

2020 ◽  
Author(s):  
Wenyu Jia ◽  
Siwan Luo ◽  
Gena Lai ◽  
Shiqi Li ◽  
Shuai Huo ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Bladder Cancer ◽  
Western Blot ◽  
Cancer Cells ◽  
Activated Macrophages ◽  
Tnf Α ◽  
Bladder Cancer Cells ◽  
And Migration ◽  
Mesenchymal Transformation ◽  
M1 Type

Abstract BackgroundPolyporus polysaccharide (PPS), an active ingredient of traditional Chinese medicinal Polyporus umbellatus, has multiple biological functions, such as anti-cancer, immune-regulating and hepatoprotective activities. The purpose of this study was to investigate the mechanism of PPS activated macrophages in the treatment of bladder cancer.Methods100 ng/mL Phorbol myristate acetate (PMA) was used to induce THP-1 human leukemic cells as a macrophage model. Flow cytometry was used to detect the expression of CD14 and CD68 to verify the establishment of macrophage model. After that, Macrophages derived from THP-1 were treated with different concentrations of PPS (1,10 and 100 ug/mL). Flow cytometry and RT-PCR were used to detected the expression of CD16, CD23, CD86, CD40 and interleukin (IL)-Iβ, iNOS mRNA. ELISA was used to test the change of IL-1β and TNF-α in macrophage after the treatment with PPS. The conditioned medium from PPS-polarized macrophages was used to detect the effect of activated macrophages on bladder cancer. MTT assay, 5-ethynyl-2¢-deoxyuridine assay, flow cytometry, Transwell assay, and Western blot analysis were used to detect the effects of polarized macrophages on the viability, proliferation, apoptosis, and migration of bladder cancer cells. Western blot was also used to analysis the change of JAK2/NF-κB pathway protein.ResultsPPS promoted the expression of pro-inflammatory factors, such as IL-Iβ, TNF-α and iNOS, and surface molecules CD86, CD16, CD23, and CD40 in macrophages and then polarized macrophages to M1 type. The results demonstrated that activated macrophages inhibited the proliferation of bladder cancer cells, regulated their apoptosis, and inhibited migration and epithelial–mesenchymal transformation (EMT). JAK2/NF-κB pathways were downregulated in the anti-bladder cancer process of activated macrophages. ConclusionThe findings indicated that PPS inhibited the proliferation and progression of bladder cancer by the polarization of macrophages to M1 type, and JAK2/NF-κB pathway was downregulated in the process of anti-bladder cancer.

scholarly journals BET inhibitor JQ1 suppresses cell proliferation via inducing autophagy and activating LKB1/AMPK in bladder cancer cells

2019 ◽  
Vol 8 (10) ◽  
pp. 4792-4805 ◽  
Author(s):  
Feng Li ◽  
Chao Yang ◽  
Hai‐Bao Zhang ◽  
Jianbin Ma ◽  
Jing Jia ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cancer Cells ◽  
Bet Inhibitor ◽  
Bladder Cancer Cells

scholarly journals Vitamin K2 Induces Mitochondria-Related Apoptosis in Human Bladder Cancer Cells via ROS and JNK/p38 MAPK Signal Pathways

PLoS ONE ◽  
2016 ◽  
Vol 11 (8) ◽  
pp. e0161886 ◽  
Author(s):  
Fengsen Duan ◽  
Yuejin Yu ◽  
Rijian Guan ◽  
Zhiliang Xu ◽  
Huageng Liang ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
P38 Mapk ◽  
Vitamin K2 ◽  
Signal Pathways ◽  
Human Bladder Cancer ◽  
Human Bladder ◽  
Bladder Cancer Cells ◽  
Human Bladder Cancer Cells

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.

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