Department of Urology, Sijhih Cathay General Hospital, New Taipei City, Taiwan; Department of Mechanical Engineering, National Central University, Jhongli, Taiwan; School of Medicine, Fu Jen Catholic University, New Taipei City, Taiwan.
Department of Mechanical Engineering, National Central University, Jhongli, Taiwan; Institute of Biomedical Engineering, National Central University, Jhongli, Taiwan.
Urol Oncol. 2014 Jan;32(1):26.e17-24. doi: 10.1016/j.urolonc.2012.09.004. Epub 2013 Feb 9.
Urothelial carcinoma (UC) of the bladder is the second most common cancer of the genitourinary system. Clinical UC treatment usually involves transurethral resection of the bladder tumor followed by adjuvant intravesical immunotherapy or chemotherapy to prevent recurrence. Intravesical chemotherapy induces fewer side effects than immunotherapy but is less effective at preventing tumor recurrence. Improvement to intravesical chemotherapy is, therefore, needed.
Cellular effects of mitomycin C (MMC) and hydrostatic pressure on UC BFTC905 cells were assessed. The viability of the UC cells was determined using cellular proliferation assay. Changes in apoptotic function were evaluated by caspase 3/7 activities, expression of FasL, and loss of mitochondrial membrane potential.
Reduced cell viability was associated with increasing hydrostatic pressure. Caspase 3/7 activities were increased following treatment of the UC cells with MMC or hydrostatic pressure. In combination with 10 kPa hydrostatic pressure, MMC treatment induced increasing FasL expression. The mitochondria of UC cells displayed increasingly impaired membrane potentials following a combined treatment with 10 μg/ml MMC and 10 kPa hydrostatic pressure.
Both MMC and hydrostatic pressure can induce apoptosis in UC cells through an extrinsic pathway. Hydrostatic pressure specifically increases MMC-induced apoptosis and might minimize the side effects of the chemotherapy by reducing the concentration of the chemical agent. This study provides a new and alternative approach for treatment of patients with UC following transurethral resection of the bladder tumor.
膀胱癌是泌尿系统中第二大常见的癌症。临床膀胱癌的治疗通常包括经尿道膀胱肿瘤切除术，然后辅助膀胱内免疫治疗或化疗，以防止复发。膀胱内化疗比免疫治疗引起的副作用少，但预防肿瘤复发的效果较差。因此，需要改进膀胱内化疗。
评估丝裂霉素 C（MMC）和静水压力对 UC BFTC905 细胞的细胞作用。通过细胞增殖测定法测定 UC 细胞的活力。通过 caspase 3/7 活性、FasL 表达和线粒体膜电位丧失来评估凋亡功能的变化。
随着静水压力的增加，细胞活力降低。用 MMC 或静水压力处理 UC 细胞后， caspase 3/7 活性增加。与 10 kPa 静水压力联合治疗可诱导 FasL 表达增加。与 10μg/ml MMC 和 10 kPa 静水压力联合治疗后，UC 细胞的线粒体膜电位越来越受损。
MMC 和静水压力均可通过外源性途径诱导 UC 细胞凋亡。静水压力可特异性增加 MMC 诱导的细胞凋亡，并通过减少化学药物浓度来最小化化疗的副作用。这项研究为经尿道膀胱肿瘤切除术治疗膀胱癌患者提供了一种新的替代方法。
