Su Jin Lee1, Bok-Nam Park1, Jung Hyun Roh1, Young-Sil An1, Hoon Hur2, Joon-Kee Yoon3. 1. Department of Nuclear Medicine and Molecular Imaging, Ajou University School of Medicine, Suwon, Republic of Korea. 2. Department of Surgery, Ajou University School of Medicine, Suwon, Republic of Korea. 3. Department of Nuclear Medicine and Molecular Imaging, Ajou University School of Medicine, Suwon, Republic of Korea jkyoon3@ajou.ac.kr.
Abstract
AIM: We assessed the effect of cell-cycle synchronization using the T-type calcium channel inhibitor mibefradil on the anticancer effects of 2-deoxy-D-glucose (2-DG) and glucose metabolism in breast cancer cells. MATERIALS AND METHODS: MDA-MB-231 cells were treated with mibefradil, followed by 2-DG with/without paclitaxel, then cells were assessed for viability. Glucose metabolism was evaluated by 3H-2-DG uptake, lactate concentration, and membrane glucose transporter 1 expression after mibefradil treatment. RESULTS: Viability was significantly lower in cells receiving the combination therapy of mibefradil and 2-DG relative to 2-DG treatment alone; addition of paclitaxel to the combination therapy further reduced the viability of breast cancer cells. Withdrawal of mibefradil resulted in a significant increase in cellular 3H-2-DG uptake uptake, a slight accumulation of lactate, and increased membrane glucose transporter 1 expression. CONCLUSION: Mibefradil-induced cell-cycle synchronization enhanced the anticancer activity of 2-DG in breast cancer cells due to an increase in cellular glucose metabolism. Copyright
AIM: We assessed the effect of cell-cycle synchronization using the T-type calcium channel inhibitor mibefradil on the anticancer effects of 2-deoxy-D-glucose (2-DG) and glucose metabolism in breast cancer cells. MATERIALS AND METHODS: MDA-MB-231 cells were treated with mibefradil, followed by 2-DG with/without paclitaxel, then cells were assessed for viability. Glucose metabolism was evaluated by 3H-2-DG uptake, lactate concentration, and membrane glucose transporter 1 expression after mibefradil treatment. RESULTS: Viability was significantly lower in cells receiving the combination therapy of mibefradil and 2-DG relative to 2-DG treatment alone; addition of paclitaxel to the combination therapy further reduced the viability of breast cancer cells. Withdrawal of mibefradil resulted in a significant increase in cellular 3H-2-DG uptake uptake, a slight accumulation of lactate, and increased membrane glucose transporter 1 expression. CONCLUSION:Mibefradil-induced cell-cycle synchronization enhanced the anticancer activity of 2-DG in breast cancer cells due to an increase in cellular glucose metabolism. Copyright