CAJ | 학술논문

目的：通过建立过表达PC-1的前列腺癌LNCaP细胞系及敲低PC-1表达的C4-2细胞系，探究PC-1激活AKT信号通路的分子机制。方法：将PC-1基因及针对PC-1的siRNA序列，分别克隆至慢病毒表达载体pCDH-EF1-Myc-MCS-T2A-Puro及干扰载体pSIH1-H1-Puro，包装成慢病毒后分别感染前列腺癌LNCaP及C4-2细胞，通过Western印迹鉴定PC-1过表达及敲低效果，并检测PI3K/AKT/mTOR信号通路相关蛋白S6K、AKT的磷酸化水平。结果：PC-1过表达时，S6K磷酸化水平下降，而AKT的磷酸化水平上升。结论：PC-1可以通过抑制S6K激酶活性，解除其对AKT的负反馈抑制作用，从而激活AKT激酶的活性。
목적：통과건립과표체PC-1적전렬선암LNCaP세포계급고저PC-1표체적C4-2세포계，탐구PC-1격활AKT신호통로적분자궤제。방법：장PC-1기인급침대PC-1적siRNA서렬，분별극륭지만병독표체재체pCDH-EF1-Myc-MCS-T2A-Puro급간우재체pSIH1-H1-Puro，포장성만병독후분별감염전렬선암LNCaP급C4-2세포，통과Western인적감정PC-1과표체급고저효과，병검측PI3K/AKT/mTOR신호통로상관단백S6K、AKT적린산화수평。결과：PC-1과표체시，S6K린산화수평하강，이AKT적린산화수평상승。결론：PC-1가이통과억제S6K격매활성，해제기대AKT적부반궤억제작용，종이격활AKT격매적활성。
Objective: To construct a prostate cancer LNCaP cell line stably overexpressing PC-1 and a C4-2 cell line in which PC-1 expression is stably knocked down and to explore how PC-1 active AKT pathway. Meth-ods: PC-1 and siRNA primers targeting PC-1 were separately cloned into the control vector pCDH-EF1-MCS-T2A-Puro and pSIH1-H1-Puro. Prostate cancer cells LNCaP and C4-2 cells were infected with lentivirus and the expression of PC-1 was identified by Western blot. Meanwhile, Western blot was performed to detect the phosphor-ylation level of PI3K/AKT/mTOR pathway associated proteins such as S6K, AKT. Results: PC-1 overexpression can decrease the S6K phosphorylation level, while increase AKT phophorylation level. Conclusion: PC-1 may ac-tive AKT kinase in some way through releasing negative feedback regulation of S6K on the PI3K/AKT pathway.