Glucose Metabolism in the Progression of Prostate Cancer

被引:107
作者
Cutruzzola, Francesca [1 ]
Giardina, Giorgio [1 ]
Marani, Marina [1 ]
Macone, Alberto [1 ]
Paiardini, Alessandro [2 ]
Rinaldo, Serena [1 ]
Paone, Alessio [1 ]
机构
[1] Sapienza Univ Rome, Dept Biochem Sci A Rossi Fanelli, Rome, Italy
[2] Sapienza Univ Roma, Dept Biol & Biotechnol Charles Darwin, Rome, Italy
关键词
prostate cancer; metabolism; microenvironment; Warburg effect; inflammation; BONE-MARROW; MITOCHONDRIAL ACONITASE; TUMOR-GROWTH; ZINC UPTAKE; KAPPA-B; CELLS; INFLAMMATION; ADIPOSE; ACID; FIBROBLASTS;
D O I
10.3389/fphys.2017.00097
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Prostate cancer is one of the most common types of cancer in western country males but the mechanisms involved in the transformation processes have not been clearly elucidated. Alteration in cellular metabolism in cancer cells is recognized as a hallmark of malignant transformation, although it is becoming clear that the biological features of metabolic reprogramming not only differ in different cancers, but also among different cells in a type of cancer. Normal prostate epithelial cells have a peculiar and very inefficient energy metabolism as they use glucose to synthesize citrate that is secreted as part of the seminal liquid. During the transformation process, prostate cancer cells modify their energy metabolism from inefficient to highly efficient, often taking advantage of the interaction with other cell types in the tumor microenvironment that are corrupted to produce and secrete metabolic intermediates used by cancer cells in catabolic and anabolic processes. We recapitulate the metabolic transformations occurring in the prostate from the normal cell to the metastasis, highlighting the role of the microenvironment and summarizing what is known on the molecular mechanisms involved in the process.
引用
收藏
页数:8
相关论文
共 50 条
[31]  
Palsson-McDermott EM, 2015, CELL METAB, V21, P65, DOI [10.1016/j.cmet.2014.12.005, 10.1016/j.cmet.2015.01.017]
[32]   Lactate Transporters in the Context of Prostate Cancer Metabolism: What Do We Know? [J].
Pertega-Gomes, Nelma ;
Baltazar, Fatima .
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 2014, 15 (10) :18333-18348
[33]   A lactate shuttle system between tumour and stromal cells is associated with poor prognosis in prostate cancer [J].
Pertega-Gomes, Nelma ;
Vizcaino, Jose R. ;
Attig, Jan ;
Jurmeister, Sarah ;
Lopes, Carlos ;
Baltazar, Fatima .
BMC CANCER, 2014, 14
[34]  
Rishi I, 2003, APPL IMMUNOHISTO M M, V11, P253
[35]   Positron emission tomography for prostate, bladder, and renal cancer [J].
Schöder, H ;
Larson, SM .
SEMINARS IN NUCLEAR MEDICINE, 2004, 34 (04) :274-292
[36]   Prostate cancer and inflammation: the evidence [J].
Sfanos, Karen S. ;
De Marzo, Angelo M. .
HISTOPATHOLOGY, 2012, 60 (01) :199-215
[37]   Targeting lactate-fueled respiration selectively kills hypoxic tumor cells in mice [J].
Sonveaux, Pierre ;
Vegran, Frederique ;
Schroeder, Thies ;
Wergin, Melanie C. ;
Verrax, Julien ;
Rabbani, Zahid N. ;
De Saedeleer, Christophe J. ;
Kennedy, Kelly M. ;
Diepart, Caroline ;
Jordan, Benedicte F. ;
Kelley, Michael J. ;
Gallez, Bernard ;
Wahl, Miriam L. ;
Feron, Olivier ;
Dewhirst, Mark W. .
JOURNAL OF CLINICAL INVESTIGATION, 2008, 118 (12) :3930-3942
[38]   Cancer heterogeneity is not compatible with one unique cancer cell metabolic map [J].
Strickaert, A. ;
Saiselet, M. ;
Dom, G. ;
De Deken, X. ;
Dumont, J. E. ;
Feron, O. ;
Sonveaux, P. ;
Maenhaut, C. .
ONCOGENE, 2017, 36 (19) :2637-2642
[39]  
Strotmeyer Elsa S, 2007, Curr Opin Endocrinol Diabetes Obes, V14, P429, DOI 10.1097/MED.0b013e3282f1cba3
[40]   Breast Cancer Cell Colonization of the Human Bone Marrow Adipose Tissue Niche [J].
Templeton, Zach S. ;
Lie, Wen-Rong ;
Wang, Weiqi ;
Rosenberg-Hasson, Yael ;
Alluri, Rajiv V. ;
Tamaresis, John S. ;
Bachmann, Michael H. ;
Lee, Kitty ;
Maloney, William J. ;
Contag, Christopher H. ;
King, Bonnie L. .
NEOPLASIA, 2015, 17 (12) :849-861