CAJ | 학술논문

目的：观察骨髓间充质干细胞（BMSCs）来源的外泌体（exosome）对小鼠乳腺癌细胞4T1增殖、侵袭的影响，并探讨其可能机制。方法将小鼠乳腺癌细胞4T1随机分为3组，4T1＋vehicle组仅加入400μL无血清培养基，4T1＋exosome组加入400μL由无血清培养基配置的exosome，4T1＋exosome＋磷脂酰肌醇3激酶（ PI3K）／Akt信号通路阻断剂（ Y294002）组加入400μL终浓度为5μmol／mL Y294002及400μg／mL exosome的培养基。分别采用MTT法、细胞划痕实验、Western blotting法检测各组细胞增殖、迁移和侵袭能力以及PI3K／Akt信号通路相关蛋白。结果4T1＋exosome组、4T1＋vehicle组、4T1＋exosome＋Y294002组细胞增殖抑制率分别为0．713％±0．050％、0．401％±0．030％、0．459％±0．800％，4T1＋exosome组分别与4T1＋vehicle组、4T1＋exosome＋Y294002组比较，P均＜0．05。4T1＋exosome组、4T1＋vehicle组、4T1＋exosome＋Y294002组细胞迁移距离分别为（388．0±36．1）、（295．0±34．2）、（275．0±63．5）μm，4T1＋exosome组分别与4T1＋vehicle组、4T1＋exosome＋Y294002组比较，P均＜0．05。4T1＋exosome组p-AKT、β-catenin OD值分别为0．30±0．11、0．30±0．08，4T1＋vehicle组分别为1．10±0．41、0．70±0．08，4T1＋exosome＋Y294002组分别为0．40±0．13、0．30±0．07，4T1＋exosome组分别与4T1＋vehicle组、4T1＋exosome＋Y294002组比较，P均＜0．05。结论 BMSCs来源的exosome能够增加小鼠乳腺癌细胞4T1的增殖、迁移及侵袭能力，其机制可能与上调PI3K／Akt信号通路有关。
목적：관찰골수간충질간세포（BMSCs）래원적외비체（exosome）대소서유선암세포4T1증식、침습적영향，병탐토기가능궤제。방법장소서유선암세포4T1수궤분위3조，4T1＋vehicle조부가입400μL무혈청배양기，4T1＋exosome조가입400μL유무혈청배양기배치적exosome，4T1＋exosome＋린지선기순3격매（ PI3K）／Akt신호통로조단제（ Y294002）조가입400μL종농도위5μmol／mL Y294002급400μg／mL exosome적배양기。분별채용MTT법、세포화흔실험、Western blotting법검측각조세포증식、천이화침습능력이급PI3K／Akt신호통로상관단백。결과4T1＋exosome조、4T1＋vehicle조、4T1＋exosome＋Y294002조세포증식억제솔분별위0．713％±0．050％、0．401％±0．030％、0．459％±0．800％，4T1＋exosome조분별여4T1＋vehicle조、4T1＋exosome＋Y294002조비교，P균＜0．05。4T1＋exosome조、4T1＋vehicle조、4T1＋exosome＋Y294002조세포천이거리분별위（388．0±36．1）、（295．0±34．2）、（275．0±63．5）μm，4T1＋exosome조분별여4T1＋vehicle조、4T1＋exosome＋Y294002조비교，P균＜0．05。4T1＋exosome조p-AKT、β-catenin OD치분별위0．30±0．11、0．30±0．08，4T1＋vehicle조분별위1．10±0．41、0．70±0．08，4T1＋exosome＋Y294002조분별위0．40±0．13、0．30±0．07，4T1＋exosome조분별여4T1＋vehicle조、4T1＋exosome＋Y294002조비교，P균＜0．05。결론 BMSCs래원적exosome능구증가소서유선암세포4T1적증식、천이급침습능력，기궤제가능여상조PI3K／Akt신호통로유관。
Objective To observe the influence of bone marrow mesenchymal stem cells ( BMSCs)-derived exosome on the proliferation and invasion of mouse breast cancer cells 4T1 and to investigate the mechanism.Methods The mouse breast cancer cells 4T1 were randomly divided into three groups:4T1+vehicle group, 4T1+exosome group and 4T1+exosome+Y294002 (an inhibitor of PI3K/Akt signaling pathway) group.4T1+vehicle group was added with 400μL se-rum-free medium, 4T1+exosome group was added with 400 μL serum-free medium containing 400 μg/mL exosome and 4T1+exosome+Y294002 group was added with 400 μL serum-free medium containing 400 μg/mL exosome and 5 μg/mL Y294002.We used the MTT, cell scratch test and Western blotting to examine the effect of BMSCs-derived exosome on the proliferation, migration and invasion abilities as well as the PI3K/Akt signaling pathway of 4T1 cells.Results The in-hibition rates of cell proliferation of 4T1+vehicle group, 4T1+exosome group and 4T1+exosome+Y294002 group were 0.713%±0.05%, 0.401%±0.03%and 0.459%±0.80%, respectively.Significant difference was found between 4T1+exosome group and 4T1+vehicle group, 4T1+exosome+Y294002 group (all P<0.05).The cell migration distance of 4T1+vehicle group, 4T1+exosome group and 4T1+exosome+Y294002 group was (388.0 ±36.1), (295.0 ± 34.2) and (275.0 ±63.5) μm, respectively.Significant difference was found between 4T1+exosome group and 4T1+vehicle group, 4T1+exosome+Y294002 group (all P<0.05).The OD values of p-AKT and β-catenin of 4T1+exo-some group were 0.3 ±0.11 and 0.3 ±0.08, they were 1.1 ±0.41 and 0.7 ±0.08 in 4T1+vehicle group, 0.4 ±0.13 and 0.3 ±0.07 in the 4T1+exosome+Y294002 group.Significant difference was found between 4T1+exosome group and 4T1+vehicle group, 4T1+exosome+Y294002 group (all P<0.05).Conclusion BMSCs-derived exosome can promote the proliferation, migration and invasion abilities of mouse breast cancer cells 4T1, which may be related to the up-regulation of PI3K/Akt signaling pathway.