Madka Venkateshwar, Mohammed Altaf, Li Qian, Zhang Yuting, Kumar Gaurav, Lightfoot Stan, Wu Xueru, Steele Vernon, Kopelovich Levy, Rao Chinthalapally V
Center for Cancer Prevention and Drug Development, Stephenson Cancer Center, Department of Medicine, Hematology-Oncology Section, University of Oklahoma Health Sciences Center Oklahoma City, OK, USA.
Department of Urology, NYU Medical Center NY, USA.
Am J Cancer Res. 2015 Sep 15;5(10):3030-41. eCollection 2015.
Mutations of the tumor suppressor p53 and elevated levels of polyamines are known to play key roles in urothelial tumorigenesis. We investigated the inhibition of polyamines biosynthesis and the restoration of p53 signaling as a possible means of preventing muscle invasive urothelial tumors using DFMO, an ODC-inhibiting agent, and CP-31398 (CP), a p53 stabilizing agent. Transgenic UPII-SV40T male mice at 6weeks age (n=15/group) were fed control diet (AIN-76A) or experimental diets containing DFMO (1000 and 2000 ppm) or 150 ppm CP or both. At 40 weeks of age, all mice were euthanized and urinary bladders were evaluated to determine tumor weight and histopathology. Low-dose DFMO had a moderate significant inhibitory effect on tumor growth (38%, P<0.02) and tumor invasion (23%). High-dose DFMO had a 47% tumor inhibition (P<0.0001) and 40% inhibition tumor invasion. There was no significant difference between 1000 and 2000 ppm doses of DFMO (P>0.05). CP at 150 ppm alone had a strong inhibitory effect on tumor growth by 80% (P<0.0001); however, no effect on tumor invasion was observed. Interestingly, the combination of DFMO (1000 ppm) and CP (150 ppm) led to significant decrease in tumor weight (70%, P<0.0001) and tumor invasion (62.5%; P<0.005). Molecular analysis of the urothelial tumors suggested a modulation of polyamine biosynthesis, proliferation, cell cycle regulators resulting from the use of these agents. These results suggest that targeting two or more pathways could be an effective approach for chemoprevention. A combination of CP and DFMO appears to be a promising strategy for urothelial TCC prevention.
已知肿瘤抑制因子p53的突变和多胺水平升高在尿路上皮肿瘤发生中起关键作用。我们研究了抑制多胺生物合成和恢复p53信号传导作为预防肌肉浸润性尿路上皮肿瘤的一种可能手段,使用鸟氨酸脱羧酶(ODC)抑制剂二氟甲基鸟氨酸(DFMO)和p53稳定剂CP-31398(CP)。给6周龄的转基因UPII-SV40T雄性小鼠(每组n = 15)喂食对照饮食(AIN-76A)或含有DFMO(1000和2000 ppm)或150 ppm CP或两者的实验饮食。在40周龄时,对所有小鼠实施安乐死,并对膀胱进行评估以确定肿瘤重量和组织病理学。低剂量DFMO对肿瘤生长有中度显著抑制作用(38%,P<0.02),对肿瘤侵袭有23%的抑制作用。高剂量DFMO对肿瘤的抑制率为47%(P<0.0001),对肿瘤侵袭的抑制率为40%。1000 ppm和2000 ppm剂量的DFMO之间无显著差异(P>0.05)。单独使用150 ppm的CP对肿瘤生长有80%的强烈抑制作用(P<0.0001);然而,未观察到对肿瘤侵袭有影响。有趣的是,DFMO(1000 ppm)和CP(150 ppm)联合使用导致肿瘤重量显著降低(70%,P<0.0001)和肿瘤侵袭显著降低(62.5%;P<0.005)。对尿路上皮肿瘤的分子分析表明,使用这些药物可调节多胺生物合成、增殖和细胞周期调节因子。这些结果表明,针对两条或更多途径可能是化学预防的有效方法。CP和DFMO联合使用似乎是预防尿路上皮移行细胞癌的一种有前景的策略。