Being polycyclic hydrocarbon, cholesterol has the quality for making DNA
adduct within cell nucleus. Structurally cholesterol and its epoxide are very close to
polycyclic carcinogenic precursor e.g. benzo-alpha-pyrene, which is well known for its
carcinogenic pulse by forming adduct to chromosomal DNA. In fact normal cross
membrane transports of cholesterol, either on cell surface or on nuclear membrane turn
desynchronized in cancer tumor cells. A cholesterol loaded cell nucleus has been
correlated to wobbly cell cycle operation and aberrant cell proliferation in many cancer
type viz. leukemia, breast carcinoma, prostate carcinoma etc. A reprogrammed
cholesterol metabolism affects tumor associated immune cell activity, cellular
apoptosis and kinetics of cell survival. In fact, cholesterol concentration within cell
nucleus has been found correlated with cellular life span. In tumor microenvironment
intracellular cholesterol concentration varies from one to another cell type. While it
increases within tumor cells, the surrounding immune cells die because of scarcity of
intracellular cholesterol concentration. Intervention of this biphasic role of cholesterol
in and around the cancer tumor could be a model target for anti-cancer therapeutic
management.
Keywords: Anti-cancer therapy, Breast cancer, Carcinogenesis, Cholesterol
homeostasis, Leukemia, Low density lipoprotein, Low density lipoprotein
receptor, Metformin, Nuclear cholesterol, Peripheral type benzodiazepine
receptor, PD-1, PD-L1, Polycyclic hydrocarbon, Prostate cancer, Statin.