Abstract
Metabolic changes during malignant transformation have been noted for many years in tumours. Otto Warburg first reported that cancer cells preferentially rely on glycolysis for energy production, even in the presence of oxygen, leading to the production of high levels of lactate. The crucial role of lactate efflux and exchange within the tumour microenvironment drew attention to monocarboxylate transporters (MCTs). MCTs have been recognized as promising targets in cancer therapy, and their expression was described in a large variety of tumours; however, studies showing how these isoforms contribute to the acquisition of the malignant phenotype are scarce and still unclear regarding prostate cancer. In this review, we focus on the role for MCTs in cell metabolism, supporting the development and progression of prostate cancer, and discuss the exploitation of the metabolic nature of prostate cancer for therapeutic and diagnostic purposes.
Highlights
Prostate cancer (PCa) is the most diagnosed malignancy in men and the second leading cause of cancer-related death in the USA [1]
It was characterized by heterologous expression in Xenopus laevis oocytes, exhibiting the highest Km values for most substrates and inhibitors when compared to MCT1 and MCT2 [43]
We found that alterations in the expression of metabolism-related proteins were already evident in the early stages of malignant transformation, suggesting the continuing alteration of cancer associated fibroblasts (CAFs) from an early stage
Summary
Prostate cancer (PCa) is the most diagnosed malignancy in men and the second leading cause of cancer-related death in the USA [1]. Many putative risk factors, including hormones, dietary factors, obesity, physical inactivity, occupation, vasectomy, smoking, sexual factors and genetic susceptibility, have been implicated, but the epidemiologic evidence is not conclusive While it is not known whether the risk factors explaining the observed patterns are environmental, lifestyle or genetic, it is likely that a complex interplay of these factors is associated with PCa development. There are some available methods frequently used for PCa detection, their performance is sub-optimal due to non-satisfactory sensitivity and specificity rates. In this context, new therapeutic strategies, as well as new biomarkers are urgently needed, for early detection, and as ancillary tools for diagnosis, which is still based on the histopathological evaluation of biopsy specimens [3,4,5,6,7]
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