CAJ | 학술논문

卵巢透明细胞癌（OCCC）是上皮性卵巢癌的一种特殊组织学类型，对传统的化疗方案耐药，预后不良，寻找新的靶向治疗方案迫在眉睫。磷脂酰肌醇3激酶/蛋白激酶B/哺乳动物雷帕霉素靶体蛋白（PI3K/AKT/mTOR）信号通路在卵巢癌的发生和发展中发挥重要作用，并且与化疗耐药密切相关。该通路的活化不但可以抑制细胞凋亡，促进细胞增殖，还参与肿瘤的侵袭与转移。在OCCC中，PI3K/AKT/mTOR信号通路中的多种蛋白表达异常，该通路中的受体及激酶可能成为治疗OCCC的潜在靶点。现有研究表明PI3K/AKT/mTOR通路抑制剂不仅能增加紫杉醇或顺铂的细胞毒性效应，还可影响OCCC细胞系的生长情况。特别是OCCC中最常见的AT丰富结合域1A（ARID1A）突变与PI3K/AKT/mTOR信号通路关系十分密切。因此，针对PI3K/AKT/mTOR信号通路开发新的靶向治疗药物可能对OCCC的治疗具有一定意义。综述该通路与OCCC的关系，以期为探索新的靶向治疗提供理论基础。
란소투명세포암（OCCC）시상피성란소암적일충특수조직학류형，대전통적화료방안내약，예후불량，심조신적파향치료방안박재미첩。린지선기순3격매/단백격매B/포유동물뢰파매소파체단백（PI3K/AKT/mTOR）신호통로재란소암적발생화발전중발휘중요작용，병차여화료내약밀절상관。해통로적활화불단가이억제세포조망，촉진세포증식，환삼여종류적침습여전이。재OCCC중，PI3K/AKT/mTOR신호통로중적다충단백표체이상，해통로중적수체급격매가능성위치료OCCC적잠재파점。현유연구표명PI3K/AKT/mTOR통로억제제불부능증가자삼순혹순박적세포독성효응，환가영향OCCC세포계적생장정황。특별시OCCC중최상견적AT봉부결합역1A（ARID1A）돌변여PI3K/AKT/mTOR신호통로관계십분밀절。인차，침대PI3K/AKT/mTOR신호통로개발신적파향치료약물가능대OCCC적치료구유일정의의。종술해통로여OCCC적관계，이기위탐색신적파향치료제공이론기출。
Ovarian clear cell carcinoma (OCCC) is a special histological subtype of epithelial ovarian cancer, and presents resistant to the traditional chemotherapy on-hand, resulting in poor prognosis, so looking for a novel targeted therapy is extremely urgent. PI3K/AKT/mTOR pathway plays a significant role in the process of occurrence and development of ovarian cancer, and is intimately related to the resistance of chemotherapy. The suppression of apoptosis, the promotion of cell proliferation and the migration of tumor can be enforced by the pathway activation. The various proteins in PI3K/AKT/mTOR pathways express anomaly in the OCCC frequently, and thus the special receptor and kinase of the pathway could be a potential target for the therapy of ovarian clear cell carcinoma. The increasing of paclitaxel or cis-platinum cytotoxic effection and the growth of OCCC are in touch with PI3K/AKT/mTOR pathways in available studies. As the most frequent mutation in OCCC, ARID1A is especially related to PI3K/AKT/mTOR pathways. Therefore, to search for novel targeted drug to the pathway may benefit the treatment of OCCC to some extent. To lay a theory fundation of the new targeted treatment, the relationship of this pathway and OCCC will be interpreted in this paper.