Desferrithiocin is a more potent antineoplastic agent than desferrioxamine

Desferrithiocin (DFT) is an orally effective Fe chelator, with a similar high affinity and selectivity for Fe to desferrioxamine (DFO), which has been shown clinically to possess antineoplastic activity. In this study, DFT was assessed for antineoplastic potential in hepatocellular carcinoma cell li...

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Main Authors: Kicic, Anthony, Chua, A.C.G., Baker, E.
Format: Journal Article
Language:English
Published: NATURE PUBLISHING GROUP 2002
Subjects:
Online Access:http://hdl.handle.net/20.500.11937/76835
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author Kicic, Anthony
Chua, A.C.G.
Baker, E.
author_facet Kicic, Anthony
Chua, A.C.G.
Baker, E.
author_sort Kicic, Anthony
building Curtin Institutional Repository
collection Online Access
description Desferrithiocin (DFT) is an orally effective Fe chelator, with a similar high affinity and selectivity for Fe to desferrioxamine (DFO), which has been shown clinically to possess antineoplastic activity. In this study, DFT was assessed for antineoplastic potential in hepatocellular carcinoma cell lines (HCC). This was done as there are few treatments for this aggressive neoplasm. The effects of DFT on cell proliferation, cell cycle progression, Fe uptake and toxicity were examined. To establish whether DFT was selective for cancer cells a comparison was made with normal (non-proliferating) hepatocytes and non-tumorigenic (proliferating) fibroblasts (SWISS-3T3). DFT was a potent inhibitor of HCC proliferation (IC50∼40 μM). DFO also inhibited HCC proliferation under the same conditions, but was much less active (IC50 = 110-210 μM). When saturated with Fe, the activity of DFT, like DFO, was greatly diminished, suggesting it may act by depriving the cells of Fe or inactivating essential Fe pool(s). Indeed DFT rapidly decreased Fe uptake from Tf-59Fe by hepatoma cells and also by normal hepatocytes. However, DFT (and DFO) had much less effect on cell survival in hepatocytes and fibroblasts than in hepatoma cells. DFT may, like DFO, inhibit the cell cycle in the S phase of DNA synthesis. Both chelators showed low toxicity. These results indicate that DFT has potent antineoplastic activity in HCC. Further investigation into the DFT class of Fe chelators seems warranted, particularly in view of its high activity in relation to DFO, a chelator which is already in clinical trial for neuroblastoma.
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spelling curtin-20.500.11937-768352019-11-14T01:50:39Z Desferrithiocin is a more potent antineoplastic agent than desferrioxamine Kicic, Anthony Chua, A.C.G. Baker, E. Science & Technology Life Sciences & Biomedicine Pharmacology & Pharmacy desferrithiocin desferrioxamine Fe chelators Fe uptake hepatocellular carcinoma EFFECTIVE ANTIPROLIFERATIVE AGENTS ISONICOTINOYL HYDRAZONE CLASS NEUROBLASTOMA CELL-LINES IRON CHELATORS ANTINEUROBLASTOMA ACTIVITY HEPATOCELLULAR-CARCINOMA TRANSFERRIN UPTAKE CYTO-TOXICITY TUMOR-CELLS D-CECAT Desferrithiocin (DFT) is an orally effective Fe chelator, with a similar high affinity and selectivity for Fe to desferrioxamine (DFO), which has been shown clinically to possess antineoplastic activity. In this study, DFT was assessed for antineoplastic potential in hepatocellular carcinoma cell lines (HCC). This was done as there are few treatments for this aggressive neoplasm. The effects of DFT on cell proliferation, cell cycle progression, Fe uptake and toxicity were examined. To establish whether DFT was selective for cancer cells a comparison was made with normal (non-proliferating) hepatocytes and non-tumorigenic (proliferating) fibroblasts (SWISS-3T3). DFT was a potent inhibitor of HCC proliferation (IC50∼40 μM). DFO also inhibited HCC proliferation under the same conditions, but was much less active (IC50 = 110-210 μM). When saturated with Fe, the activity of DFT, like DFO, was greatly diminished, suggesting it may act by depriving the cells of Fe or inactivating essential Fe pool(s). Indeed DFT rapidly decreased Fe uptake from Tf-59Fe by hepatoma cells and also by normal hepatocytes. However, DFT (and DFO) had much less effect on cell survival in hepatocytes and fibroblasts than in hepatoma cells. DFT may, like DFO, inhibit the cell cycle in the S phase of DNA synthesis. Both chelators showed low toxicity. These results indicate that DFT has potent antineoplastic activity in HCC. Further investigation into the DFT class of Fe chelators seems warranted, particularly in view of its high activity in relation to DFO, a chelator which is already in clinical trial for neuroblastoma. 2002 Journal Article http://hdl.handle.net/20.500.11937/76835 10.1038/sj.bjp.0704507 English NATURE PUBLISHING GROUP restricted
spellingShingle Science & Technology
Life Sciences & Biomedicine
Pharmacology & Pharmacy
desferrithiocin
desferrioxamine
Fe chelators
Fe uptake
hepatocellular carcinoma
EFFECTIVE ANTIPROLIFERATIVE AGENTS
ISONICOTINOYL HYDRAZONE CLASS
NEUROBLASTOMA CELL-LINES
IRON CHELATORS
ANTINEUROBLASTOMA ACTIVITY
HEPATOCELLULAR-CARCINOMA
TRANSFERRIN UPTAKE
CYTO-TOXICITY
TUMOR-CELLS
D-CECAT
Kicic, Anthony
Chua, A.C.G.
Baker, E.
Desferrithiocin is a more potent antineoplastic agent than desferrioxamine
title Desferrithiocin is a more potent antineoplastic agent than desferrioxamine
title_full Desferrithiocin is a more potent antineoplastic agent than desferrioxamine
title_fullStr Desferrithiocin is a more potent antineoplastic agent than desferrioxamine
title_full_unstemmed Desferrithiocin is a more potent antineoplastic agent than desferrioxamine
title_short Desferrithiocin is a more potent antineoplastic agent than desferrioxamine
title_sort desferrithiocin is a more potent antineoplastic agent than desferrioxamine
topic Science & Technology
Life Sciences & Biomedicine
Pharmacology & Pharmacy
desferrithiocin
desferrioxamine
Fe chelators
Fe uptake
hepatocellular carcinoma
EFFECTIVE ANTIPROLIFERATIVE AGENTS
ISONICOTINOYL HYDRAZONE CLASS
NEUROBLASTOMA CELL-LINES
IRON CHELATORS
ANTINEUROBLASTOMA ACTIVITY
HEPATOCELLULAR-CARCINOMA
TRANSFERRIN UPTAKE
CYTO-TOXICITY
TUMOR-CELLS
D-CECAT
url http://hdl.handle.net/20.500.11937/76835