ABSTRACT
This study examined the effect of silencing LRIG3 expression on the proliferation and apoptosis of bladder cancer T24 cells and explored the role of LRIG3 in the tumorigenesis of bladder cancer.Bladder cancer T24 cells were routinely cultured and pSilencer plasmids were employed to construct LRIG3 eukaryotic expression vector of LRIG3-siRNA,i.e.,pSilencer-LRIG3-siRNA.After confirmation,the vector was transfected into HEK293 cells to make a replication-deficient adenovirus,pAd-LRIG3-siRNA,which was then introduced into bladder cancer T24 cells.RT-PCR,Western-blotting were performed to detect the levels of LRIG3 mRNA and proteins.Cells number was determined by using MTT test.Hoechst33258 staining,transmission microscopy,flow cytometery were conducted to examine the cell apoptosis.Three groups included a blank control group,a negative control group (containing non-interfering plasmids) and a pAd-LRIG3-siRNA group.Our results showed that the recombinant pAd-LRIG3-siRNA was successfully transfected into the bladder cancer T24 cells.The siRNA formed by the transcription of the recombinant plasmids resulted in significantly reduced expressions of LRIG3 gene and protein and significantly decreased cell proliferation and growth in the pAd-LRIG3-siRNA group as compared with the control group (P＜0.01).The siRNA also caused apoptotic changes of some cells,with the apoptosis rate being (17.69±0.75)％,which was significantly different from that of the control group (P＜0.01).It was concluded that recombinant pAd-LRIG3-siRNA plasmids could effectively decrease the expression of LRIG3 mRNA and proteins and,to some extent,inhibit the proliferation and promote the apoptosis of bladder cancer T24 cells.Silencing LRIG3 gene might be a novel alternative for the treatment of bladder cancer.
ABSTRACT
The correlation between the anatomic site of spinal cord injury and real-time conditions of bladder and urethral function was assessed in order to provide a reasonable basis for the clinical treat-ment of neurogenic bladder. A total of 134 patients with spinal cord injuries (105 males, 29 females;averaged 34.1 years old) were involved in this retrospective analysis, including urodynamic evaluation,clinical examination and imaging for anatomical position, and Bors-Comarr classification. The associa-tions between the levels of injury and urodynamic findings were analyzed. The results showed that mean follow-up duration was 16.7 months (range 8-27 months). Complete spinal cord injuries occurred in 21 cases, and incomplete spinal cord injuries in 113 cases. Of the 43 patients with upper motor neu-ron (UMN) injuries, hyperreflexia and (or) detmsor sphincter dyssynergia were demonstrated in 30 (69.8%), 31 (72.1%) suffered low bladder compliance (less than 12.5 mL/cmH2O), 28 (65.1%) had high detrusor leak point pressures (greater than 40 cmH2O), and 34 (79.1%) had residual urine. Of the 91 pa-tients with lower motor neuron (LMN) injuries, areflexia occurred in 78 (85.7%), high compliance in 75 (82.4%), low leak point pressures in 80 (87.9%), and residual urine in 87 (95.6%), respectively. The as-sociations between the anatomical site of spinal cord injury and urodynamic findings were ill defined. In patients with spinal cord injury, this study revealed a significant association between the level of injury and the type of voiding dysfunction. The anatomical site of spinal cord injury can not be predicted in real-time condition of bladder and urethral function. Management of neurogenic bladder in patients with spinal cord injury must be based on urodynamic findings rather than inferences from the neurologic evaluation.