Breast cancer is the most common type of cancer in women, and colon cancer is the third most common cancer in both sexes and the second leading cause of cancer deaths worldwide . The majority of cancer patients, however, will not decease because of their primary tumor, but rather because of the spreading of metastasis, which is responsible for over 90% of cancer deaths .
The prevalence of obesity has increased dramatically over the last four decades, and it can be considered the leading health problem of the developed countries in the 21st century. Obesity is strongly associated with the development of diabetes mellitus type 2 (DM2) and co-morbid diseases, such as hypertension and hyperlipidemia, commonly summarized as the metabolic syndrome .
Up-to-date retrospective and prospective epidemiological studies showed strong correlations between the metabolic syndrome and the incidence of malignant neoplasms in different organs [4, 5]. Obesity increases the risk of breast and colon cancer [6, 7]. DM2 is directly associated with a higher incidence and faster progression of several neoplasms including colon and breast cancer [5, 8]. In particular, increased fasting serum insulin concentrations, commonly found in DM2 patients, seem to increase the risk for breast and colon cancer [9, 10]. Besides, tyrosine kinases, namely the insulin receptor (IR) and insulin-like growth factor (IGF) receptors, are over-expressed in several human cancers, including cancer of the breast . Consequently, over-expression of these receptors yields a selective growth advantage to breast cancer cells, especially in the presence of insulin resistance and associated hyperinsulinemia . It has been known for over two decades that glucose is the driving force for tumor cell growth  and that high levels of insulin promote metastasis .
Insulin operates by binding to its target cell receptor, a heterotetrameric, transmembrane, multisubunit glycoprotein. The insulin signal is propagated through a phosphorylation network involving intracellular molecules such as phosphoinositid-3-kinase (PI3K), protein kinase B (PKB, Akt) and phospholipase Cγ (PLCγ). The serine/threonine kinase Akt is a well known regulator of widely divergent cellular processes, and it is implicated in intracellular insulin signaling. Akt has been described as an oncogene in several human cancers [15, 16], and it is known to be a promoter of tumor cell proliferation , prolonged cell survival [18, 19], and angiogenesis . The phosphorylation and thus activation of Akt can be specifically inhibited by the trifluoroacetate salt hydrate A6730 . Phospholipases (PLCs) are tyrosine kinase substrates that provide diacylglycerols (DAGs) for intracellular signaling in various contexts and its isoform PLCγ is known to be implicated in intracellular insulin signaling  and in colon and breast cancer progression [23, 24]. U73122 is an aminosteroid that specifically inhibits PLCγ activation .
Given this knowledge about the gravity of glucose metabolism in tumor cells on the one hand and the growing number of studies investigating the epidemiological connection between the metabolic syndrome/DM2 and the development and progression of several human cancers on the other hand, surprisingly little is known about the underlying molecular changes and mechanisms that facilitate tumor development and progression when excessive glucose and insulin are available.
For these reasons, we report about the regulatory functions of Akt and PLCγ regarding tumor cell proliferation and migration under the specific premise of higher than normal glucose and insulin concentrations.