[摘要] 目的：探讨miR-103a-3p 在乳腺癌组织及血清中的表达及其作用机制。方法：选用2017 年3 月1 日至2017 年8 月31日在海南医学院第二附属医院肿瘤外科手术切除、经病理确诊为乳腺癌的31 例癌组织及对应的21 例癌旁组织标本、38 例乳腺癌患者及22 例健康体检者的血清标本，以及乳腺癌细胞系MCF-7 和MDA-MB-231，分别利用慢病毒载体pHBLV-U6-Luc-T2A-Puro和PLL3.7 敲低乳腺癌细胞系MCF-7 和MDA-MB-231 中的miR-103a-3p 和PDK4，qPCR法和Western blotting 法检测miR-103a-3p和PDK4 在癌组织、血清及乳腺癌细胞系中mRNA和蛋白的表达，CCK-8 细胞增殖实验检测转染的乳腺癌细胞MCF-7 和MDAMB-231 的细胞增殖水平，用Olympus AU5400 检测葡萄糖消耗与乳酸生成。结果：乳腺癌患者组织和血清中miR-103a-3p 表达水平均显著低于癌旁组织（P<0.01，P<0.05）。敲低miR-103a-3p 后，乳腺癌细胞系MCF-7 和MDA-MB-231 中葡萄糖消耗（P<0.01）与乳酸生成增多（P<0.01）、细胞增殖增强（P<0.01）、PDK4 表达上调（P<0.01）；在miR-103a-3p 沉默的MCF-7 和MDA-MB-231 细胞中，敲低PDK4 导致减弱葡萄糖消耗（P<0.01）、乳酸生成（P<0.01）和细胞增殖（P<0.01）。结论：乳腺癌细胞中miR-103a-3p 通过抑制PDK4减弱糖酵解活动，从而抑制乳腺癌细胞增殖。

[Abstract] Objective：To explore miR-103a-3p expression in the tumor tissues and the serum of breast cancer patients, and its role and mechanism in breast cancer development. Methods: Pathologically confirmed 31 cases of tumor tissues and 21 cases of para-cancerous tissues resected at Department of Oncological Surgery of the Second Affiliated Hospital of Hainan Medical University (Haikou, China)from March 1, 2017 to August 31，2017 were collected for this study; in addition, serum samples from 38 breast cancer patients and 22 healthy subjects as well as the breast cancer cell lines MCF-7 and MDA-MB-231 were used in this study. pHBLV-U6-Luc-T2A-Puro and PLL3.7 lentivirus were applied to knock down miR-103a-3p and PDK4 in MCF-7 and MDA-MB-231 cells, respectively. qPCR and Western blotting were performed to examine the mRNA and protein expressions of miR-103a-3p and PDK4 in tissues and serums of breast cancer patients as well as the in cell lines, respectively; CCK-8 assay was applied to detect the proliferation of MCF-7 and MDAMB-231 cells; Olympus AU5400 was applied to detect the glucose consumption and lactate production in indicated cell line. Results：miR-103a-3p was significantly decreased in tumor tissues compared with the paracancerous tissues (P<0.01). miR-103a-3p knockdown activated the glucos consumption and lactate production (all P<0.01), increased the PKD4 expression (P<0.01) in MCF-7 and MDAMD-231 cells, and promoted the proliferation of MCF-7 and MDA-MB-231 cells (P<0.01). Furthermore, knockdown of PDK4 suppressed the glucose consumption, lactate production and proliferation in MCF-7 and MDA-MB-231 cells with miR-103a-3p silencing (all P<0.01). Conclusion：In the breast cancer, miR-103a-3p inhibited the proliferation of breast cancer cells through down-regulation of PDK4 and PDK4-mediated aerobic glycolysis.

海南省卫生厅科研项目（No. 2011-73）；海南省重点研发计划资助项目（No. ZDYF2017087）