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Targeting Cellular Metabolism Chemosensitizes the Doxorubicin-Resistant Human Breast Adenocarcinoma Cells.
Biomed Res Int. 2015; 2015:453986.BR

Abstract

Metabolic energy preferentially produced by glycolysis was an advantageous metabolic phenotype of cancer cells. It is also an essential contributor to the progression of multidrug resistance in cancer cells. By developing human breast cancer MCF-7 cells resistant to doxorubicin (DOX) (MCF-7/MDR cells), the effects and mechanisms of 2-deoxy-D-glucose (2DG), a glucose analogue, on reversing multidrug resistance were investigated. 2DG significantly inhibited the viability of MCF-7/MDR cells and enhanced DOX-induced apoptosis by upregulating protein expression of AMPKα, P53, and caspase-3. The study demonstrated that energy restriction induced by 2DG was relevant to the synergistic effect of 2DG and DOX. The proteins of multidrug gene (the MDR-related protein, MRP1) and P-glycoprotein (P-gp) in MCF-7/MDR cells were downregulated after exposure to 2DG, accompanied with the suppression of the activity of ATP-dependent drug-efflux pump and transmembrane transporter, increasing the intracellular accumulation of DOX to reverse the chemoresistance in multidrug cancer cells.

Authors+Show Affiliations

Training Center of Medical Experiments, Basic Medical School, Fudan University, Shanghai 200032, China.Department of Oncology, Shanghai Xuhui Central Hospital, Shanghai 200031, China.Training Center of Medical Experiments, Basic Medical School, Fudan University, Shanghai 200032, China.Institute of Radiation Medicine, Fudan University, Shanghai 200032, China.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26558272

Citation

Ma, Shulan, et al. "Targeting Cellular Metabolism Chemosensitizes the Doxorubicin-Resistant Human Breast Adenocarcinoma Cells." BioMed Research International, vol. 2015, 2015, p. 453986.
Ma S, Jia R, Li D, et al. Targeting Cellular Metabolism Chemosensitizes the Doxorubicin-Resistant Human Breast Adenocarcinoma Cells. Biomed Res Int. 2015;2015:453986.
Ma, S., Jia, R., Li, D., & Shen, B. (2015). Targeting Cellular Metabolism Chemosensitizes the Doxorubicin-Resistant Human Breast Adenocarcinoma Cells. BioMed Research International, 2015, 453986. https://doi.org/10.1155/2015/453986
Ma S, et al. Targeting Cellular Metabolism Chemosensitizes the Doxorubicin-Resistant Human Breast Adenocarcinoma Cells. Biomed Res Int. 2015;2015:453986. PubMed PMID: 26558272.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Targeting Cellular Metabolism Chemosensitizes the Doxorubicin-Resistant Human Breast Adenocarcinoma Cells. AU - Ma,Shulan, AU - Jia,Rongfei, AU - Li,Dongju, AU - Shen,Bo, Y1 - 2015/10/19/ PY - 2015/06/27/received PY - 2015/09/25/revised PY - 2015/09/29/accepted PY - 2015/11/12/entrez PY - 2015/11/12/pubmed PY - 2016/8/27/medline SP - 453986 EP - 453986 JF - BioMed research international JO - Biomed Res Int VL - 2015 N2 - Metabolic energy preferentially produced by glycolysis was an advantageous metabolic phenotype of cancer cells. It is also an essential contributor to the progression of multidrug resistance in cancer cells. By developing human breast cancer MCF-7 cells resistant to doxorubicin (DOX) (MCF-7/MDR cells), the effects and mechanisms of 2-deoxy-D-glucose (2DG), a glucose analogue, on reversing multidrug resistance were investigated. 2DG significantly inhibited the viability of MCF-7/MDR cells and enhanced DOX-induced apoptosis by upregulating protein expression of AMPKα, P53, and caspase-3. The study demonstrated that energy restriction induced by 2DG was relevant to the synergistic effect of 2DG and DOX. The proteins of multidrug gene (the MDR-related protein, MRP1) and P-glycoprotein (P-gp) in MCF-7/MDR cells were downregulated after exposure to 2DG, accompanied with the suppression of the activity of ATP-dependent drug-efflux pump and transmembrane transporter, increasing the intracellular accumulation of DOX to reverse the chemoresistance in multidrug cancer cells. SN - 2314-6141 UR - https://www.unboundmedicine.com/medline/citation/26558272/Targeting_Cellular_Metabolism_Chemosensitizes_the_Doxorubicin_Resistant_Human_Breast_Adenocarcinoma_Cells_ L2 - https://doi.org/10.1155/2015/453986 DB - PRIME DP - Unbound Medicine ER -