LINC00346 regulates glycolysis by modulation of glucose transporter 1 in breast cancer cells |
| |
| Institution: | 1. Department of Pharmacy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China;2. Department of Otolaryngology-Head and Neck Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China;1. School of Public Health, Sun Yat-sen University, Guangzhou 510080, China;2. The First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, China;3. The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou 510630, China;1. State Key Laboratory of Bioreactor Engineering & Shanghai Key Laboratory of New Drug Design, School of pharmacy, East China University of Science and Technology, Shanghai, PR China;2. State Key Laboratory of Bioreactor Engineering, Shanghai Key Laboratory of Chemical Biology, School of Pharmacy, East China University of Science and Technology, Shanghai, PR China;1. Department of Breast Surgery, Jilin Tumor Hospital, Jilin, 130012, PR China;2. Department of Thoracic Neoplasms, Jilin Tumor Hospital, Jilin, 130012, PR China;3. Department of Oncology, Jilin Tumor Hospital, Jilin, 130012, PR China |
| |
| Abstract: | Most cancer cells preferentially metabolize glucose by glycolysis rather than oxidative phosphorylation to proliferate efficiently. LncRNAs have been proposed as crucial regulators in pathophysiological processes including cell growth, apoptosis and glucose metabolism. However, little is known regarding the specific role of LINC00346 in regulating glucose metabolism in breast cancer. LINC00346 and miR-148a/b expression in breast cancer cells was detected by qRT-PCR. The relationships between LINC00346, glucose transporter 1 (GLUT1) and miR-148a/b in breast cancer cells were explored by luciferase reporter assay. Cell proliferation and apoptosis were evaluated by CCK-8 and flow cytometry analysis, respectively. Glycolysis was detected by measuring the glucose uptake and lactate production. Results showed that LINC00346 was over-expressed while miR-148a/b was low-expressed in breast cancer cells. miR-148a/b were direct targets of LINC00346 in breast cancer cells. LINC00346 knockdown inhibited cell proliferation and glycolysis, and induced apoptosis by upregulating miR-148a/b in breast cancer cells. Furthermore, we found that LINC00346 knockdown repressed GLUT1 expression in breast cancer cells by upregulating miR-148a/b. In conclusion, LINC00346 knockdown suppressed breast cancer cell glycolysis by upregulating miR-148a/b and repressing GLUT1 expression. |
| |
| Keywords: | LINC00346 miR-148a/b GLUT1 Glycolysis Breast cancer |
| 本文献已被 ScienceDirect 等数据库收录！ |
|
