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.

Autocrine CCL2 promotes cell migration and invasion via PKC activation and tyrosine phosphorylation of paxillin in bladder cancer cells

Cytokine ◽  
2012 ◽  
Vol 59 (2) ◽  
pp. 423-432 ◽  
Author(s):  
Hsiao-Ying Chiu ◽  
Kuang-Hui Sun ◽  
Shiow-Yi Chen ◽  
Hsiao-Hsien Wang ◽  
Ming-Yung Lee ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Tyrosine Phosphorylation ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Bladder Cancer Cells ◽  
Pkc Activation

scholarly journals MicroRNA-124-3p inhibits cell migration and invasion in bladder cancer cells by targeting ROCK1

2013 ◽  
Vol 11 (1) ◽  
pp. 276 ◽  
Author(s):  
Xianglai Xu ◽  
Shiqi Li ◽  
Yiwei Lin ◽  
Hong Chen ◽  
Zhenghui Hu ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Bladder Cancer Cells ◽  
Microrna 124

2-(3-Methoxyphenyl)-6, 7-methylenedioxoquinolin-4-one, a novel synthetic compound, inhibited migration and invasion in TSGH8301 human bladder cancer cells

2010 ◽  
Vol 30 (8) ◽  
pp. 1045-1052 ◽  
Author(s):  
Kuang-Chi Lai ◽  
Shu-Chun Hsu ◽  
Jai-Sing Yang ◽  
Chao-Lin Kuo ◽  
Siu-Wan Ip ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Boyden Chamber ◽  
Human Bladder Cancer ◽  
Human Bladder ◽  
Synthetic Compound ◽  
Cell Migration And Invasion ◽  
Cell Proliferation Inhibition

Matrix metalloproteinases (MMPs) play an important role in the invasion, metastasis and angiogenesis of cancer cells. Many agents have been shown to inhibit the cancer cell migration and invasion by suppression of MMPs. 2-(3-Methoxyphenyl)-6,7-methylenedioxoquinolin-4-one (MMEQ) is a derivative compound synthesized from quinolin and the purpose of this study is to determine whether or not cell migration would be reduced in human bladder cancer TSGH8301 cells after MMEQ treatment. Wound healing assay and boyden chamber assay were used in cell migration and invasion determinations. Cell migration and invasion inhibited by MMEQ exerted an inhibitory effect on the sevenless homolog-1 (SOS-1), protein kinase c (PKC), extracellular signal-regulated kinase (ERK) and Rho A for causing the inhibitions of MMP-2 and -9, and then followed by the inhibitions of invasion and migration. MMEQ also affected FAK, PI3K or inhibited growth factor receptor-bound protein 2 (GRB2), nuclear factor kappaB (NF-κB), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) for cell proliferation inhibition. Therefore, MMEQ may serve as a drug in the prevention of tumor metastasis of bladder cancer in the future.

scholarly journals MiR-20a-5p Negatively Regulates NR4A3 to Promote Metastasis in Bladder Cancer

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Haibei Yang ◽  
Zhao Chen ◽  
Zhiming Liu
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Suppressor Gene ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Regulatory Relationship ◽  
Carcinogenic Effect ◽  
Invasion And Migration ◽  
Bladder Cancer Cells ◽  
And Migration

Metastasis is the leading cause of death in cancer patients. Therefore, the prediction and treatment of metastasis are critical in improving the survival of patients with bladder cancer. In this study, we aimed to investigate the role of miR-20a-5p and NR4A3 in bladder cancer and the regulatory relationship between them. The high expression of miR-20a-5p in the bladder cancer (BCa) tissues and cells was determined by qRT-PCR. Exogenous miR-20a-5p overexpression promoted the proliferation, migration, and invasion of BCa cells. MiR-20a-5p inhibition inhibited the BCa cell proliferation, invasion, and migration. NR4A3 was proved to be the target gene of miR-20a-5p by the double luciferase reporter assay. In addition, the reduction of NR4A3 could promote the proliferation, invasion, and clonal formation of the bladder cancer cells 5637 and T24. NR4A3 overexpression could reverse the carcinogenic effect of miR-20a. We further confirmed that the oncogenic effect of miR-20a was achieved by promoting EMT in tumor cells. MiR-20a-5p promoted the growth and metastasis of the bladder cancer cells by inhibiting the expression of the tumor suppressor gene NR4A3 and played a carcinogenic role in BCa. Thus, miR-20a-5p may become a potential therapeutic target for BCa treatment.

scholarly journals miR-1-3p Contributes to Cell Proliferation and Invasion by Targeting Glutaminase in Bladder Cancer Cells

2018 ◽  
Vol 51 (2) ◽  
pp. 513-527 ◽  
Author(s):  
Junfeng Zhang ◽  
Longsheng Wang ◽  
Shiyu Mao ◽  
Mengnan Liu ◽  
Wentao Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Methylation Status ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Bladder Cancer Cells ◽  
Cancer Tissues

Background/Aims: Increasing evidence showed that miR-1-3p plays a major role in malignant tumor progression. However, the specific biological function of miR-1-3p in bladder cancer is yet unknown. Methods: The expression levels of miR-1-3p in bladder cancer tissues and cell lines were examined by qRT-PCR. Bisulfite sequencing PCR was used for DNA methylation analysis. The target of miR-1-3p was validated by a dual luciferase reporter assay, and the effects of miR-1-3p on phenotypic changes in bladder cancer cells were investigated in vitro and in vivo. Results: The expression of miR-1-3p in bladder cancer cells was downregulated as compared to normal SV-HUC-1 cells. Also, the expression of miR-1-3p was significantly lower in bladder cancer tissues than the corresponding non-cancerous tissues. The methylation status of CpG islands was involved in the regulation of miR-1-3p expression. miR-1-3p inhibited the bladder cancer cell proliferation, migration, and invasion by directly targeting the 3’-UTR of glutaminase. It also exerted an anti-tumor effect by negatively regulating the glutaminase in a xenograft mouse model. Furthermore, GLS depletion resulted in the prolonged expression of γH2AX. Conclusion: Taken together, these results demonstrated that miR-1-3p acts as a tumor suppressor via regulation of glutaminase expression in bladder cancer progression, and miR-1-3p might represent a novel therapeutic target for the treatment of bladder cancer.

scholarly journals TEAD4 as a Prognostic Marker Promotes Cell Migration and Invasion of Urinary Bladder Cancer via EMT

2021 ◽  
Vol Volume 14 ◽  
pp. 937-949
Author(s):  
Zhengnan Huang ◽  
Yilin Yan ◽  
Pengfei Tang ◽  
Jinming Cai ◽  
Xiangqian Cao ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cell Migration ◽  
Urinary Bladder ◽  
Prognostic Marker ◽  
Urinary Bladder Cancer ◽  
Migration And Invasion ◽  
Cell Migration And Invasion

scholarly journals Lnc-STYK1-2 regulates bladder cancer cell proliferation, migration, and invasion by targeting miR-146b-5p expression and AKT/STAT3/NF-kB signaling

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ranran Dai ◽  
Qingping Jiang ◽  
You Zhou ◽  
Ruifeng Lin ◽  
Hai Lin ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Noncoding Rnas ◽  
Bladder Cancer Cell ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Bladder Cancer Cells

Abstract Background Epigenetic modulation by noncoding RNAs substantially contributes to human cancer development, but noncoding RNAs involvement in bladder cancer remains poorly understood. This study investigated the role of long noncoding RNA (lncRNA) lnc-STYK1-2 in tumorigenesis in cancerous bladder cells. Methods Differential lncRNA and mRNA profiles were characterized by high-throughput RNA sequencing combined with validation via quantitative PCR. Bladder cancer cell proliferation was assessed through MTS, and bladder cancer cell migration and invasion were assessed through a Transwell system. The in vivo tumorigenesis of bladder cancer cells was evaluated using the cancer cell line-based xenograft model. The dual-luciferase reporter assay verified the association of miR-146b-5p with lnc-STYK1-2 and the target gene. Protein abundances and phosphorylation were detected by Western blotting. Results Alterations in lncRNA profiles, including decreased lnc-STYK1-2 expression, were detected in bladder cancer tissues compared with adjacent noncancerous tissues. lnc-STYK1-2 silencing effectively promoted proliferation, migration, and invasion in two bladder cancer cell lines, 5637 and T24, and their tumorigenesis in nude mice. lnc-STYK1-2 siRNA promoted miR-146b-5p and reduced ITGA2 expression in bladder cancer cells. Moreover, miR-146b-5p suppressed ITGA2 expression in bladder cancer cells through direct association. Also, lnc-STYK1-2 directly associated with miR-146b-5p. Finally, miR-146b-5p inhibitors abrogated the alterations in bladder cell functions, ITGA2 expression, and phosphorylation of AKT, STAT3, and P65 proteins in 5637 and T24 cells induced by lnc-STYK1-2 silencing. Conclusion lnc-STYK1-2 inhibited bladder cancer cell proliferation, migration, and tumorigenesis by targeting miR-146b-5p to regulate ITGA2 expression and AKT/STAT3/NF-kB signaling.

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