中国癌症杂志
中國癌癥雜誌
중국암증잡지
CHINA ONCOLOGY
2014年
5期
349-353
,共5页
王玉林%王彪%孟欣%巴颖
王玉林%王彪%孟訢%巴穎
왕옥림%왕표%맹흔%파영
Bcl-2相关抗凋亡基因2%蛋白酶体抑制剂%凋亡%甲状腺肿瘤
Bcl-2相關抗凋亡基因2%蛋白酶體抑製劑%凋亡%甲狀腺腫瘤
Bcl-2상관항조망기인2%단백매체억제제%조망%갑상선종류
Bcl-2-associated athanogene 2%Proteasome inhibitor%Apoptosis%Thyroid cancer
背景与目的：蛋白酶体抑制剂对不同组织来源的肿瘤均有抑制其增长和促进细胞凋亡的作用，其作用机制可能与Bcl-2相关抗凋亡基因2(Bcl-2-associated athanogene 2，BAG2)有关，本研究探讨BAG2在蛋白酶体抑制剂诱导甲状腺癌细胞凋亡中的作用。方法：选取人甲状腺未分化癌细胞系ARO、FRO、KTC1、KTC2、KTC3、8305C和8505C，分别设培养液处理空白对照组、蛋白酶体抑制剂MG132处理组；利用实时定量逆转录聚合酶链反应(quantitative real-time polymerase chain reaction，qRT-PCR)检测各组细胞BAG2 mRNA表达及MG132诱导其表达的时效性；利用蛋白质印迹法(Western blot)检测各组细胞BAG2蛋白表达。结果：MTT结果显示，FRO和KTC2细胞系对蛋白酶体抑制剂最为敏感，与空白对照组相比，MG132能不同程度的增加各种细胞BAG2 mRNA及蛋白的表达水平(P<0.01)，在FRO和KTC2细胞中，BAG2 mRNA水平较对照组增加20~25倍，蛋白质的表达水平也显著增加；时间效应实验中，敏感的FRO细胞BAG2 mRNA水平增加快，没有延迟期；并且增加的最高水平显著高于非敏感的ARO细胞(P<0.01)。结论：BAG2是由蛋白酶体抑制作用诱导产生的新型分子，在蛋白酶体抑制剂诱导的甲状腺癌细胞的死亡中起着促凋亡作用。
揹景與目的：蛋白酶體抑製劑對不同組織來源的腫瘤均有抑製其增長和促進細胞凋亡的作用，其作用機製可能與Bcl-2相關抗凋亡基因2(Bcl-2-associated athanogene 2，BAG2)有關，本研究探討BAG2在蛋白酶體抑製劑誘導甲狀腺癌細胞凋亡中的作用。方法：選取人甲狀腺未分化癌細胞繫ARO、FRO、KTC1、KTC2、KTC3、8305C和8505C，分彆設培養液處理空白對照組、蛋白酶體抑製劑MG132處理組；利用實時定量逆轉錄聚閤酶鏈反應(quantitative real-time polymerase chain reaction，qRT-PCR)檢測各組細胞BAG2 mRNA錶達及MG132誘導其錶達的時效性；利用蛋白質印跡法(Western blot)檢測各組細胞BAG2蛋白錶達。結果：MTT結果顯示，FRO和KTC2細胞繫對蛋白酶體抑製劑最為敏感，與空白對照組相比，MG132能不同程度的增加各種細胞BAG2 mRNA及蛋白的錶達水平(P<0.01)，在FRO和KTC2細胞中，BAG2 mRNA水平較對照組增加20~25倍，蛋白質的錶達水平也顯著增加；時間效應實驗中，敏感的FRO細胞BAG2 mRNA水平增加快，沒有延遲期；併且增加的最高水平顯著高于非敏感的ARO細胞(P<0.01)。結論：BAG2是由蛋白酶體抑製作用誘導產生的新型分子，在蛋白酶體抑製劑誘導的甲狀腺癌細胞的死亡中起著促凋亡作用。
배경여목적：단백매체억제제대불동조직래원적종류균유억제기증장화촉진세포조망적작용，기작용궤제가능여Bcl-2상관항조망기인2(Bcl-2-associated athanogene 2，BAG2)유관，본연구탐토BAG2재단백매체억제제유도갑상선암세포조망중적작용。방법：선취인갑상선미분화암세포계ARO、FRO、KTC1、KTC2、KTC3、8305C화8505C，분별설배양액처리공백대조조、단백매체억제제MG132처리조；이용실시정량역전록취합매련반응(quantitative real-time polymerase chain reaction，qRT-PCR)검측각조세포BAG2 mRNA표체급MG132유도기표체적시효성；이용단백질인적법(Western blot)검측각조세포BAG2단백표체。결과：MTT결과현시，FRO화KTC2세포계대단백매체억제제최위민감，여공백대조조상비，MG132능불동정도적증가각충세포BAG2 mRNA급단백적표체수평(P<0.01)，재FRO화KTC2세포중，BAG2 mRNA수평교대조조증가20~25배，단백질적표체수평야현저증가；시간효응실험중，민감적FRO세포BAG2 mRNA수평증가쾌，몰유연지기；병차증가적최고수평현저고우비민감적ARO세포(P<0.01)。결론：BAG2시유단백매체억제작용유도산생적신형분자，재단백매체억제제유도적갑상선암세포적사망중기착촉조망작용。
Background and purpose: For neoplasms with different sources, proteasome inhibitors can inhibit their growth and promote the cell apoptosis. Its mechanism may be associated with Bcl-2-associated athanogene 2 (BAG2). We aimed to investigate the involvement of in thyroid cancer cell death induced by proteasome inhibitors. Methods:A panel of thyroid cancer cells (ARO, FRO, KTC1, KTC2, KTC3, 8305C and 8505C) were treated with vehicle or proteasome inhibitor MG132;BAG2 mRNA and protein levels were analyzed using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot, respectively. Results:MTT results indicated that FRO and KTC2 cell lines were the most sensitive to proteasome inhibitors. MG132 induced BAG2 mRNA and protein expression in the panel of thyroid cancer cells with various degree (P<0.01), for FRO and KTC2 cell line, the BAG2 mRNA level was increased in 20 to 25 times, meanwhile the protein expression level also increased signiifcantly;Sensitive FRO cells demonstrated quicker induction of BAG2 compared with insensitive ARO cells. Moreover, the extents of BAG2 induction in FRO cells were higher than that in ARO cells. Conclusion: BAG2 is a novel molecule induced by proteasome inhibitor, which might function as a proapoptotic molecule in thyroid cancer cell death mediated by proteasome inhibitor.
