scholarly journals The miR-130 family promotes cell migration and invasion in bladder cancer through FAK and Akt phosphorylation by regulating PTEN

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Hiroshi Egawa ◽  
Kentaro Jingushi ◽  
Takayuki Hirono ◽  
Yuko Ueda ◽  
Kaori Kitae ◽  
...  
2019 ◽  
Vol 14 (1) ◽  
pp. 440-447
Author(s):  
Chunhui Dong ◽  
Yihui Liu ◽  
Guiping Yu ◽  
Xu Li ◽  
Ling Chen

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.


2016 ◽  
Vol 34 (2_suppl) ◽  
pp. 447-447
Author(s):  
Andrew M. Hau ◽  
Andrew Gilder ◽  
Jing-jing Hu ◽  
Steven L. Gonias ◽  
Donna E. Hansel

447 Background: Bladder cancer currently ranks as the fifth most common and the single most expensive cancer to manage in the United States. Although it is established that invasive behavior is a major predictor of diminished outcomes for patients with bladder cancer, the molecular mechanisms governing bladder cancer cell invasion are not well understood. The urokinase receptor (uPAR) and mammalian target of rapamycin complex 2 (mTORC2) represent two powerful pro-invasion candidates that have increased expression in high-grade, invasive bladder cancer, though the former has not been characterized in detail in bladder cancer. Therefore, the aims of this study are to characterize the uPAR signaling network and delineate the signaling interplay between mTORC2 and uPAR in bladder cancer. Methods: Using immunoblot and RT-qPCR analyses, we evaluated uPAR expression in a panel of immortalized bladder cancer cell lines: UROtsa, RT4, UMUC3, T24 and J82. uPAR influence on mTORC1 and mTORC2 signaling was determined by immunoblot analysis following targeted gene-silencing of uPAR using siRNA. Additionally, the effects of uPAR knockdown on cell migration and invasion were investigated using modified scratch-wound migration and transwell invasion assays. Lastly, signaling interplay between uPAR and mTORC2 was investigated by evaluating the effects of uPAR and mTORC2 silencing on Rac1 activity. Results: uPAR knockdown in a subset (T24 and J82) of invasive bladder cancer cell lines inhibited mTORC2, but not mTORC1, activity as measured by P-AKT S473 and P-S6 levels. We found that uPAR silencing in T24 and J82 cells resulted in significant reductions in cell migration and invasion through Matrigel. This is likely attributed to inhibition of Rac1 and decreased lamellipodia formation. Conclusions: Collectively, our results identify uPAR and mTORC2 as major regulators of bladder cancer cell invasion and that these two systems are linked through Rac1. Further investigation of uPAR and mTORC2 inhibition using uPAR-targeting antibodies and mTOR inhibitors in an in vivo mouse model of bladder cancer will determine if these signaling pathways are therapeutically beneficial for the treatment of bladder cancer.


2016 ◽  
Vol 36 (4) ◽  
pp. 2049-2058 ◽  
Author(s):  
Jun Wang ◽  
Xiaomei Zhao ◽  
Jianhua Shi ◽  
Yiwei Pan ◽  
Qinghai Chen ◽  
...  

2016 ◽  
Vol 45 (46) ◽  
pp. 18465-18475 ◽  
Author(s):  
Yahui Yang ◽  
Shulin Deng ◽  
Qinsong Zeng ◽  
Weilie Hu ◽  
Tianfeng Chen

Herein highly stable selenadiazole derivatives were synthesized and found to be able to induce bladder cancer cell apoptosis and inhibit cell migration and invasion through the activation of ROS-mediated pathways.


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 ◽  
...  

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