Ironjustic
Sun, May-29-05, 17:16
<<snip>> IP-6 can cause a decrease in the cellular
proliferation of Hep-2 cells <<snip>>
Biomed Sci Instrum. 2005;41:205-10. Related Articles, Links
Growth and cell viability of estradiol and IP-6 treated Hep-2
laryngeal carcinoma cells.
Dorsey M, Benghuzzi H, Tucci M, Cason Z.
University of Mississippi Medical Center, Jackson, MS
39216, USA.
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.
PMID: 15850106 [PubMed - indexed for MEDLINE]
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Who loves ya. Tom
proliferation of Hep-2 cells <<snip>>
Biomed Sci Instrum. 2005;41:205-10. Related Articles, Links
Growth and cell viability of estradiol and IP-6 treated Hep-2
laryngeal carcinoma cells.
Dorsey M, Benghuzzi H, Tucci M, Cason Z.
University of Mississippi Medical Center, Jackson, MS
39216, USA.
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.
PMID: 15850106 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------
-------------------
Who loves ya. Tom