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Page 2 of 17 Gabriele et al. J Cancer Metastasis Treat 2018;4:17 I http://dx.doi.org/10.20517/2394-4722.2018.06

Table 1. Main genes involved in prostate cancer
Gene Full name Function/references
BRCA1 Breast cancer susceptibility DNA repair [7]
protein type 1
BRCA2 Breast cancer susceptibility DNA repair [7]
protein type 2
HPC1 Hereditary prostate cancer Prostate cancer susceptibility ribonuclease L [8]
VDR Vitamin D receptor Inhibition of cell growth, metastasis and angiogenesis; apoptosis modulation and cell
differentiation [8]
CD82 Cluster of differentiation 82 Metastasis suppressor attenuates the matrix adhesion [9]
PTEN Phosphatase and tensin homolog Tumor suppressor and cell cycle regulation [9]
mTOR Mammalian target of rapamycin Key signaling pathway linked to tumorigenesis and resistance to therapy [10]
PSA Prostate specific antigen Dissolver of cervical mucus, allowing the entry of sperm in the uterus [11]
BCL2 B-cell lymphoma 2 Pro-survival protein associated with the development of androgen-independent
prostate cancer [12]
MKI67 Antigen Ki-67 Nuclear protein involved cell proliferation [13]
ERK-5 Mitogen-actvated protein kinase 7 Signaling processes of various receptor molecules. In response to extracellular signals,
this kinase translocate to the nucleus, where it regulates gene expression and activates
different transcription factors [14]
SP1 Transcription factor Sp1 Involved in many cellular processes, including cell differentiation, growth, apoptosis,
immune responses, DNA damage, and chromatin remodeling [15]
TPD52 Tumor protein 52 Unknown [16]

prostate cancer tends to develop in men over the age of fifty . Rates of detection of prostate cancers vary
[1]
widely across the world, with South and East Asia detecting less frequently than in Europe and in the
United States. Globally, it is the sixth leading cause of cancer-related death in men . More than 200,000
[2]
new cases are estimated in the United States in 2013, with a mortality rates over per 10 cases. Moreover,
there are different ways of classifying patients with prostate cancer: the tumor-node-metastases (TNM)
classification of malignant tumors evaluates the extension of the tumor, the involvement of lymph nodes and
the metastatic dissemination. The Gleason Grading system is additionally used to evaluate the prognosis of
men with prostate cancer. A Gleason score is given to prostate cancer based upon its microscopic appearance:
cancers with a higher Gleason score are more aggressive and have a worse prognosis .
[3,4]

Many factors, including genetics and diet, have been implicated in the development of this cancer. As
suggested by association studies, genetic background can contribute to prostate cancer risk with family,
race, and specific gene variants. Men who have a first-degree relative (brother or father) with prostate cancer
have twice the risk of developing the cancer, and those with two first-degree relatives affected have a fivefold
greater risk compared with men with no family history . Studies of twins in Scandinavia suggest that 40%
[5]
of prostate cancer risk can be explained by inherited factors .
[6]
A summary of the different genes implicated in prostate cancer are highlighted in Table 1 [7-16] .

METABOLISM AS A PRIVILEGED TARGET IN PROSTATE CANCER CELLS
Different metabolic targets and sub-targets in prostate cancer
The specific alterations in metabolic pathways observed in cancer cells confirm that tumors need unusual
amounts of energy and biosynthetic precursors to survive and grow .
[17]
However, the unique intermediary metabolism in prostate cancer cells is substantially different from that
found in other cancer cell types . In particular to satisfy the energy demand and to generate ATP, most
[18]
cancer cells are mainly derive energy from aerobic glycolysis . In androgen-dependent prostate cancer
[19]
cells, Warburg has demonstrated that glucose does not play a major metabolic role because LNCaP
[19]
cells, and androgen-sensitive human prostate adenocarcinoma cells widely employed in in vitro prostate
[20]
cancer studies, can even grow in presence of low glucose concentrations . Therefore, the metabolic state
[21]
of prostate cancer cells is altered to satisfy the increased demand for energy that is required to support the