The effects of IGF-1 on cellular phospholipids.

Signals are transduced across the cell membrane through a series of events that are triggered by the activation of receptors or opening of ion channels. It is evident that the stimulation of cells can elicit a series of catabolic cascades, which cause degradation of several membrane phospholipids. Several breakdown products participate directly in the intracellular signaling cascade. The objective of this study was to establish the changes in phospholipid pools of MG-63 cells in 15 and 30 minutes after stimulation with IGF-1, which is a known growth factor. After collection of the cells, methods were performed to prepare the samples for thin-layer chromatography. Silica gel plates were analyzed for each experiment for quantitative and qualitative data. The cells were also tested for alkaline phosphatase activity. The highest percent of radioactivity was within the phosphatidylcholine fraction of control cells at 15 minutes and phosphatidylserine at 30 minutes. The highest percent of radioactivity was in the phosphatidylserine fraction at 15 minutes and increased after 30 minutes in IGF-1 treated cells.

Hep-2 cellular function following either a bolus administration or continuous sustained release of IP-6.

Inositol 6-phosphate (IP-6) has demonstrated novel anti-cancer activity using several different tumor models. IP-6, or phytic acid, has antioxidant properties that directly act to inhibit cancer cell growth. In previous experiments using Hep-2 cells treated with a single treatment dose of IP-6 (1 mM) showed decreases in number only after 72 hours. The goal of this experiment was to deliver IP-6 in a sustained continuous manner for periods of 24, 48 and 72 hours to Hep-2 cancer cells and compare the changes in cell growth and morphology after a single bolus dose of IP-6. Our results indicated that IP-6 administered as a bolus dose was unable to reduce Hep-2 cell numbers after 24 hours. By 48 and 72 hours an approximate 50% increase in cell numbers were seen in the single dose treatment group. Sustained delivery of IP-6 resulted in significant reduction of cells over 48 hours. The dose of IP-6 given (1 mM) did not induce changes in cellular protein concentrations nor increase cellular membrane damage. Morphologically, the Hep-2 cell appear small, round to cuboidal in shape with dark eccentric nuclei and scant cytoplasm. After treatment with 1 mM IP-6, the cells showed evidence of degeneration with irregular cell borders and hyperchromatic nuclei. Overall, 1 mM IP-6 was unable to reduce Hep-2 cell proliferation for periods greater than 48 hours; however, further evaluation of the Hep-2 cytology revealed significant cellular degenerative changes that warrant additional studies to understand the action of IP-6.