CAJ | 학술논문

目的：研究高迁移率族蛋白（HMGB1）在上皮性卵巢癌、卵巢良性疾病及健康人血清中的表达情况及与临床治疗的关系，通过RNA干扰抑制探讨HMGB1对卵巢癌细胞增殖、迁移和侵袭的影响。方法：ELISA检测47例卵巢癌患者手术前及术后1个月血清中HMGB1表达水平，30例卵巢良性疾病患者作为良性肿瘤组，30例健康女性作为正常对照组；靶向HMGB1基因的慢病毒载体转染卵巢癌细胞，并利用RT-PCR和Western Blot方法检测干扰效果，CCK-8法检测细胞增殖情况，Transwell小室模型检测细胞侵袭迁移能力。结果：卵巢癌组HMGB1水平明显高于良性肿瘤组与正常对照组（P<0.01），卵巢癌术后HMGB1较术前明显降低（P<0.01），抑制HMGB1的表达可以降低卵巢癌细胞的增殖、侵袭、迁移能力。结论：HMGB1水平与卵巢癌进展密切相关，其表达下调可显著抑制卵巢癌细胞的增殖和迁移侵袭能力，有望对卵巢癌的临床检测及治疗提供新思路。
목적：연구고천이솔족단백（HMGB1）재상피성란소암、란소량성질병급건강인혈청중적표체정황급여림상치료적관계，통과RNA간우억제탐토HMGB1대란소암세포증식、천이화침습적영향。방법：ELISA검측47례란소암환자수술전급술후1개월혈청중HMGB1표체수평，30례란소량성질병환자작위량성종류조，30례건강녀성작위정상대조조；파향HMGB1기인적만병독재체전염란소암세포，병이용RT-PCR화Western Blot방법검측간우효과，CCK-8법검측세포증식정황，Transwell소실모형검측세포침습천이능력。결과：란소암조HMGB1수평명현고우량성종류조여정상대조조（P<0.01），란소암술후HMGB1교술전명현강저（P<0.01），억제HMGB1적표체가이강저란소암세포적증식、침습、천이능력。결론：HMGB1수평여란소암진전밀절상관，기표체하조가현저억제란소암세포적증식화천이침습능력，유망대란소암적림상검측급치료제공신사로。
Objective:The objective of this research is to study the serum level of the high-mobility group protein B1 (HMGB1) in human ovarian tumor (OvCa) and in a healthy control. This study also aims to identify different HMGB1 levels before and after sur-gery and to explore the inhibitory effect of HMGB1 gene silencing in the proliferation and invasion ability of OvCa. Methods: En-zyme-linked immunosorbent assay was used to measure the serum level of HMGB1 in OvCa patients and healthy subjects. Lentivirus vector with HMGB1 shRNA was constructed and used to infect OvCa cells. The expressions of HMGB1 mRNA and protein were test-ed by real-time PCR and Western blot. Cell proliferation was detected using the Cell Counting Kit-8 assay, whereas cell invasion and migration were detected by Transwell assay. Results:The serum level of HMGB1 was more elevated in patients with malignant diseas-es compared with individuals with benign diseases and the control groups. In the malignant group, the serum level of HMGB1 de-creased noticeably after therapy. Down-regulation of HMGB1 expression resulted in the inhibition of the biological behavior and metas-tasis of ovarian cancer cells. Conclusion: HMGB1 is closely associated with clinicopathologic features of OvCa. Knockdown of HMGB1 expression can significantly inhibit cell proliferation, cell migration, and cell invasion of OvCa. These findings indicate that HMGB1 can function as a therapeutic target for ovarian neoplasm in the future.