CAJ | 학술논문

目的：探讨磷酸化蛋白EBP50对乳腺癌细胞MCF-7细胞增殖的影响及其潜在机制研究。方法使用 pGPU6/Neo载体构建稳定敲除EBP50表达的MCF-7细胞株，使用Western blot检测乳腺癌细胞中EBP50、c-myc、p-ERK1/2以及ERK1/2的表达，使用磺酰罗丹明B染色方法检测乳腺癌细胞增殖。结果使用 pGPU6/Neo 载体可以稳定地降低MCF-7细胞中EBP50的表达，敲除EBP50可以促进乳腺癌细胞增殖，同时促进c-myc的表达，上调ERK1/2的磷酸化水平，但不影响ERK1/2的表达。结论 EBP50可以通过抑制ERK1/2活性，抑制MCF-7乳腺癌细胞增殖能力。
목적：탐토린산화단백EBP50대유선암세포MCF-7세포증식적영향급기잠재궤제연구。방법사용 pGPU6/Neo재체구건은정고제EBP50표체적MCF-7세포주，사용Western blot검측유선암세포중EBP50、c-myc、p-ERK1/2이급ERK1/2적표체，사용광선라단명B염색방법검측유선암세포증식。결과사용 pGPU6/Neo 재체가이은정지강저MCF-7세포중EBP50적표체，고제EBP50가이촉진유선암세포증식，동시촉진c-myc적표체，상조ERK1/2적린산화수평，단불영향ERK1/2적표체。결론 EBP50가이통과억제ERK1/2활성，억제MCF-7유선암세포증식능력。
Aim To investigate the relationship be-tween phosphoprotein EBP50 and the proliferation of breast cancer in MCF-7 cells. Methods The quali-fied recombinant plasmid sh-EBP50-pGPU6/Neo was transfected into MCF-7 cells with EBP50 knocking down. The expression of EBP50, c-myc, p-ERK1/2, and ERK1/2 was detected by Western blot. The prolif-eration ability of cells was detected by sulforhodamine B assay. Results The EBP50 knocking down plasmid was constructed successfully. MCF-7 cells with EBP50 knocking down had been established successfully. Knocking down of EBP50 increased the proliferation of MCF-7 significantly, and partially augmented the ex-pression of c-myc and phosphorylation of ERK1/2 . However, knocking down of EBP50 did not impact the expression of ERK1/2 . Conclusion EBP50 suppres-ses the proliferation of breast cancer cell through inhib-iting the activity of ERK1/2 in MCF-7 cell line.