Nutritional modulation of the cell cycle and breast cancer

Abstract

In the USA, breast cancer accounts for approximately 30% of all cancers diagnosed in women and is the second leading cause of cancer death in women. An understanding of the molecular genetic events governing breast cancer lead to both prevention and intervention strategies in an attempt to reduce mortality and morbidity from breast cancer. The last three decades of medical research examining the molecular pathogenesis of cancers have provided compelling evidence for the universal disruption of the cell cycle in human tumors. The importance of cell cycle control in human cancer was recognized by the recent award of the Nobel Prize to Drs Nurse and Hartwell for their discovery of the cyclins. More recent studies have demonstrated a critical interface between hormonal signaling and the cell cycle. In parallel, epidemiological studies have identified as being associated with breast cancer important dietary and environmental components that regulate hormonal signaling. This review describes the intersection of these two fields of study, which together imply a role for dietary prevention and intervention in human breast cancer perhaps through altering cell cycle components.

The insulin receptor: a new anticancer target for peroxisome proliferator-activated receptor- (PPAR ) and thiazolidinedione-PPAR agonists

“…Recently, non-genomic crosstalks between PPARg and cytoplasmic proteins, like extracellular signalregulated kinase (ERK) 1/2 and MAPK kinases, have been reported in cancer cells and functional importance has been given to the subcellular localization of PPARg (Burgermeister & Seger 2007, Papageorgiou et al 2007. However, the last three decades of medical research examining the molecular pathogenesis of cancers have provided compelling evidence for the universal disruption of the cell cycle in human tumors, and recent studies have demonstrated a critical interface between hormonal signaling and the cell cycle (Hilakivi-Clarke et al 2004). In this context, mitogens like insulin, via the IR, may promote the progression through the G1 phase by inducing competence of the cyclin D1/cyclin-dependant kinase 4 (CDK4) complex.…”

Role of retinol in protecting epithelial cell damage induced by Clostridium difficile toxin A

“…This dose was chosen based on our previous studies. In order to rule-out a proliferation component on cell migration, in some experiments 5 μg/ml of mitomycin C was added [15][16][17][18][19][20] min prior to the scraping to inhibit DNA synthesis and cell mitosis (Roche, Indianapolis, IN). In order to verify the effect of vitamin A on the migration following mechanical damage, the replacement of medium after scratching was made with standard medium or medium without glutamine (WG) with supplementation of vitamin A (0.01-100 nM) in absence of toxin A.…”

Dietary soya isoflavones and breast carcinogenesis: a perspective from a cell-culture model

“…The eukaryotic cell cycle is divided into G1, S, G2 and M phases, and there are checkpoints occurring at different phases to allow progression to the next phase. The tumour suppressor proteins p53 and pRb, cyclins and cyclin-dependent kinases (Cdk) have detrimental effects on the progression of the cell cycle, as reviewed by Hilakivi-Clarke et al (2004).…”