I've heard good things about IP-6 being a good supplement
1: World J Gastroenterol. 2006 Jul 14;12(26):4137-42.Click here to read Links
Effects of inositol hexaphosphate on proliferation of HT-29 human colon carcinoma cell line.
* Tian Y,
* Song Y.
Qingdao University Medical College, 38 Dengzhou Road, Qingdao 266021, Shandong Province, China.
[email protected].
AIM: To investigate the effects of inositol hexaphosphate (IP(6)) on proliferation of HT-29 human colon carcinoma cell line. METHODS: Cells were exposed to various concen-trations (0, 1.8, 3.3, 5.0, 8.0, 13.0 mmol/L) of IP(6) for a certain period of time. Its effect on growth of HT-29 cells was measured by MTT assay. The expressions of cell cycle regulators treated with IP(6) for 2 d were detected by immunocytochemistry. RESULTS: IP(6) inhibited the HT-29 cell growth in a dose- and time-dependent manner. Analysis of cell cycle regulator expression revealed that IP(6) reduced the abnormal expression of P53 and PCNA and induced the expression of P21. CONCLUSION: IP(6) has potent inhibitory effect on proliferation of HT-29 cells by modulating the expression of special cell cycle regulators.
PMID: 16830361 [PubMed - in process]
1: Carcinogenesis. 2004 Nov;25(11):2115-23. Epub 2004 Aug 5.Click here to read Links
Anti-angiogenic activity of inositol hexaphosphate (IP6).
* Vucenik I,
* Passaniti A,
* Vitolo MI,
* Tantivejkul K,
* Eggleton P,
* Shamsuddin AM.
Department of Medical and Research Technology, University of Maryland School of Medicine, Baltimore, MD, USA.
A significant anticancer activity of the naturally occurring carbohydrate inositol hexaphosphate (IP(6)) has been reported against numerous cancer models. Since tumors require angiogenesis for growth and metastasis, we hypothesize that IP(6) reduces tumor growth by inhibiting angiogenesis. Because angiogenesis depends on the interaction between endothelial and tumor cells, we investigated the effect of IP(6) on both. IP(6) inhibited the proliferation and induced the differentiation of endothelial cells in vitro; the growth of bovine aortic endothelial cells (BAECs) evaluated by MTT proliferation assay was inhibited in a dose-dependent manner (IC(50) = 0.74 mM). The combination of IP(6) and vasostatin, a calreticulin fragment with anti-angiogenic activity, was synergistically superior in growth inhibition than either compound. IP(6) inhibited human umbilical vein endothelial cell (HUVEC) tube formation (in vitro capillary differentiation) on a reconstituted extracellular matrix, Matrigel, and disrupted pre-formed tubes. IP(6) significantly reduced basic fibroblast growth factor (bFGF)-induced vessel formation (P < 0.01) in vivo in Matrigel plug assay. Exposure of HepG2, a human hepatoma cell line, to IP(6) for 8 h, resulted in a dose-dependent decrease in the mRNA levels of vascular endothelial growth factor (VEGF), as assessed by RT-PCR. IP(6) treatment of HepG2 cells for 24 h also significantly reduced the VEGF protein levels in conditioned medium, in a concentration-dependent manner (P = 0.012). Thus, IP(6) has an inhibitory effect on induced angiogenesis.
PMID: 15297368 [PubMed - in process]
1: Br J Haematol. 2002 Jun;117(3):577-87. Links
Effect of inositol hexaphosphate (IP(6)) on human normal and leukaemic haematopoietic cells.
* Deliliers GL,
* Servida F,
* Fracchiolla NS,
* Ricci C,
* Borsotti C,
* Colombo G,
* Soligo D.
Bone Marrow Transplantation Unit, I.R.C.C.S., Ospedale Maggiore and University of Milan, Via F. Sforza 35, 20122 Milan, Italy.
[email protected]
Inositol hexaphosphate (IP(6)), a naturally polyphosphorylated carbohydrate, has been reported to have significant in vivo and in vitro anticancer activity against numerous tumours, such as colon, prostate, breast, liver and rhabdomyosarcomas. To confirm this activity in haematological malignancies and to characterize some of the mechanisms of IP(6) action, we analysed its effects on human leukaemic cell lines and fresh chronic myelogenous leukaemia (CML) progenitor cells using a combined cellular and molecular approach. IP(6) had a dose-dependent cytotoxic effect on all of the evaluated cell lines, with accumulation in the G2M phase in two out of five cell lines tested. At the molecular level, cDNA microarray analysis after IP(6) exposure showed an extensive downmodulation of genes involved in transcription and cell cycle regulation and a coherent upregulation of cell cycle inhibitors. Furthermore, IP(6) treatment of fresh leukaemic samples of bone marrow CD34+ CML progenitor cells significantly inhibited granulocyte-macrophage colony-forming unit (CFU-GM) formation (P = 0.0062) in comparison to normal bone marrow specimens, which were not affected. No differentiating effect on HL60 cells was observed. Taken together, our results confirm the antiproliferative activity of IP(6) and suggest that it may have a specific antitumour effect also in chronic myeloid leukaemias, via active gene modulation.
PMID: 12028025 [PubMed - indexed for MEDLINE]
