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The past two decades have seen a drastic increase in obesity rates in Westernsocieties and emerging countries. As such, it has become increasingly importantto understand the molecular mechanisms by which obesity affects the risk of developingassociated co-morbidities. The present study aimed at identifying the effect ofinsulin on breast cancer and breast epithelial cells, reflective of obesity-associatedhyperinsulinaemia, as a molecular explanation for the increased risk of oestrogenreceptor-negative postmenopausal breast cancer in obese women. Both of the examinedbreast cancer cell lines (MDA‑MB-231 and SK-BR-3) showed intact insulin signalling(insulin receptor phosphorylation and activation of phosphoinositol-3 kinase andmitogen-activated protein kinase cell signalling pathways), with MDA-MB-231 cellsshowing aberrantly amplified insulin signalling. Insulin did not induce a physiologicallysignificant change in proliferation or apoptosis in either cell line. MDA-MB-231cells showed decreased cell proliferation and increased S-phase population, whileSK-BR-3 cells showed increased cyclin D and cyclin E gene expression and increasednecrosis after insulin treatment. Hyperinsulinaemia may not be a universal mechanismby which obesity affects breast cancer progression. Normal breast epithelial cells(MCF-10A) showed intact insulin signalling, increased cell proliferation and reducedapoptosis after insulin treatment, suggesting cell growth and survival-promotingeffects of insulin on these cells. Thus, hyperinsulinaemia may affect breast canceraetiology rather than progression and this finding may provide a novel molecularmechanism for the role of insulin in the promotion of increased postmenopausalbreast cancer risk in obese women.

A novel role for insulin resistance in the connection between obesity and postmenopausal breast cancer