CAJ | 학술논문

目的：探讨慢性心理应激对肿瘤发生发展的影响及其可能机制。方法将裸鼠随机分成应激组及对照组，每组10只；两组均皮下注射SKOV3细胞建立荷人卵巢癌皮下移植瘤模型。应激组裸鼠采用束缚应激法进行应激，构建荷人卵巢癌裸鼠慢性心理应激模型；而对照组整个实验中不接受应激。观察两组移植瘤的生长状况；采用蛋白组学方法筛选、鉴定、验证应激组与对照组移植瘤之间的差异蛋白；分析典型差异表达蛋白与肿瘤生长的可能联系。结果应激组裸鼠的移植瘤生长速度比对照组快，最终瘤重（1.717±0.571） g明显高于对照组的（1.083±0.286）g（P＜0.05）；两组移植瘤中存在数百种差异表达蛋白，有20个蛋白质斑点变化超过2倍，其中Prdx1和Prdx3蛋白在应激组中表达上调极其明显（ P＜0.05）。结论慢性心理应激可能是通过Prdx1激活NF－κB通路促进卵巢癌的进展，Prdx1和Prdx3可能成为治疗卵巢癌的靶点。
목적：탐토만성심리응격대종류발생발전적영향급기가능궤제。방법장라서수궤분성응격조급대조조，매조10지；량조균피하주사SKOV3세포건립하인란소암피하이식류모형。응격조라서채용속박응격법진행응격，구건하인란소암라서만성심리응격모형；이대조조정개실험중불접수응격。관찰량조이식류적생장상황；채용단백조학방법사선、감정、험증응격조여대조조이식류지간적차이단백；분석전형차이표체단백여종류생장적가능련계。결과응격조라서적이식류생장속도비대조조쾌，최종류중（1.717±0.571） g명현고우대조조적（1.083±0.286）g（P＜0.05）；량조이식류중존재수백충차이표체단백，유20개단백질반점변화초과2배，기중Prdx1화Prdx3단백재응격조중표체상조겁기명현（ P＜0.05）。결론만성심리응격가능시통과Prdx1격활NF－κB통로촉진란소암적진전，Prdx1화Prdx3가능성위치료란소암적파점。
Objective To investigate the role of psychological stress in carcinogenesis and progression of ovarian cancer.Methods Nude mice were randomly divided into stress and control groups (n=10).Ovarian carcinoma xeno-graft model was established using SKOV3 subcutaneously injection in both stress and control groups.Stress mouse models were constructed using the restraint stress method in stress group.The growth of xenograft was observed.The differentially expressed proteins between stress group and control group were located, identified, and verified by proteomics methods. Combined with preliminary experiments, the possible associations between typical different expression proteins and tumor growth were analyzed.Results The growth of xenograft in stress group was faster than that in control group, with signifi-cantly heavier tumor weight (1.717 ±0.571 g vs 1.083 ±0.286 g, P<0.05).There were hundreds of differentially ex-pressed proteins in xenograft between stress group and control group, as 20 protein spots were changed by over two times, among which Prdx1 and Prdx3 proteins were significantly up-regulated in stress group (P<0.05).Conclusion Chronic psychological stress could promote the progression of ovarian carcinoma activating NF-κB pathway via Prdx1, suggesting Prdx1 and Prdx3 as potential targets for the treatment of ovarian cancer.