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Archive > Volume 25 Issue 5 > 2018,25(5):490-496. DOI:10.3872/j.issn.1007-385X.2018.05.009 Prev Next
Clinical Research
Expression of miR-103a-3p in breast cancer tissues and its suppression on glycolysis and proliferation of breast cancer cells via down-regulating PDK4
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Abstract:
[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.
Keywords:
breast cancer ; MCF-7cells ; MDA-MB-231 cells ; miR-103a-3p ; PDK4 ; aerobic glycolysis ; cell proliferation
Project Supported:
Project supported by the Health Department of Hainan Province（No. 2011-73）, and the Key Research and Development Plan of Hainan Province（No. ZDYF2017087）
