English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Inositol hexaphosphate (IP(6)) is a major constituent of most cereals, legumes, nuts, oil seeds and soybean. Previous studies reported the anticancer effect of IP(6) and suggested that co-treatment of IP(6) with inositol may enhance anticancer effect of IP(6). Although the anticancer effect of IP(6) has been intensively studied, the combinational effect of IP(6) and inositol and involved mechanisms are not well understood so far. In the present study, we investigated the effect of IP(6) and myo-inositol (MI) on cell cycle regulation and apoptosis using PC3 prostate cancer cell lines. When cells were co-treated with IP(6) and MI, the extent of cell growth inhibition was significantly increased than that by IP(6) alone. To identify the effect of IP(6) and MI on apoptosis, the activity of caspase-3 was measured. The caspase-3 activity was significantly increased when cells were treated with either IP(6) alone or both IP(6) and MI, with no significant enhancement by co-treatment. To investigate the effect of IP(6) and MI of cell cycle arrest, we measured p21 mRNA expression in PC3 cells and observed significant increase in p21 mRNA by IP(6). But synergistic regulation by co-treatment with IP(6) and MI was not observed. In addition, there was no significant effect by co-treatment compared to IP(6) treatment on the regulation of cell cycle progression although IP(6) significantly changed cell cycle distribution in the presence of MI or not. Therefore, these findings support that IP(6) has anticancer function by induction of apoptosis and regulation of cell cycle. However, synergistic effect by MI on cell cycle regulation and apoptosis was not observed in PC3 prostate cancer cells.

Apoptotic effect of IP6was not enhanced by co-treatment with myo-inositol in prostate carcinoma PC3 cells

Apoptotic effect of IP₆was not enhanced by co-treatment with myo-inositol in prostate carcinoma PC3 cells