Growth and cell viability of estradiol and IP-6 treated Hep-2 laryngeal carcinoma cells.

Inositol 6-phosphate (IP-6) has demonstrated novel anti-cancer activity using several different tumor models. IP-6, a phytoestrogen, has estrogen receptor (ER) binding capabilities that are not known to cause cellular proliferation in hormone sensitive cells. It is hypothesized that IP6 can induce competitive inhibition with estrogen for estrogenic binding sites on cancer cells resulting in decreased proliferation. In this experiment, Hep-2 cells were treated with Estradiol and IP-6 in a dose dependant manner for 24, 48, and 72 hours. They were analyzed for changes in number, protein concentrations, damage, and morphology. There was an increase in cell proliferation in Estradiol treated Hep-2 cells. Cells treated with IP-6 showed no change in cell proliferation in the 24 or 48-hour groups, but there was a decrease in number with the 72-hour group, particularly with the 1mM dose. Both the Estradiol and IP-6 treatments caused no membrane oxidation and the level of protein synthesis stayed consistent. The morphology showed small round to cuboidal, single cells with scant, dense, basophilic cytoplasm and hyperchromatic nuclei with smooth borders. Some cells showed anucleation and cellular degeneration. Although IP-6 is a phytoestrogen, the results show that affinity for estrogen binding sites on Hep-2 cells is greatly decreased. However, with time given increased concentrations, IP-6 can cause a decrease in the cellular proliferation of Hep-2 cells without initiating cellular apoptosis.