Triparanol

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Hong Zhao - One of the best experts on this subject based on the ideXlab platform.

  • Triparanol suppresses human tumor growth in vitro and in vivo
    Biochemical and Biophysical Research Communications, 2012
    Co-Authors: Xinyu Bi, Fang Zhang, Miao He, Yi Zhang, Hong Zhao
    Abstract:

    Highlights: Black-Right-Pointing-Pointer Demonstrate Triparanol can block proliferation in multiple cancer cells. Black-Right-Pointing-Pointer Demonstrate Triparanol can induce apoptosis in multiple cancer cells. Black-Right-Pointing-Pointer Proved Triparanol can inhibit Hedgehog signaling in multiple cancer cells. Black-Right-Pointing-Pointer Demonstrated Triparanol can impede tumor growth in vivo in mouse xenograft model. -- Abstract: Despite the improved contemporary multidisciplinary regimens treating cancer, majority of cancer patients still suffer from adverse effects and relapse, therefore posing a significant challenge to uncover more efficacious molecular therapeutics targeting signaling pathways central to tumorigenesis. Here, our study have demonstrated that Triparanol, a cholesterol synthesis inhibitor, can block proliferation and induce apoptosis in multiple human cancer cells including lung, breast, liver, pancreatic, prostate cancer and melanoma cells, and growth inhibition can be rescued by exogenous addition of cholesterol. Remarkably, we have proved Triparanol can significantly repress Hedgehog pathway signaling in these human cancer cells. Furthermore, study in a mouse xenograft model of human lung cancer has validated that Triparanol can impede tumor growth in vivo. We have therefore uncovered Triparanol as potential new cancer therapeutic in treating multiple types of human cancers with deregulated Hedgehog signaling.

V M K Venho - One of the best experts on this subject based on the ideXlab platform.

  • drug absorption from the small intestine of the Triparanol treated rat in situ
    Pharmacology & Toxicology, 2009
    Co-Authors: V M K Venho
    Abstract:

    The effect of treatment with Triparanol (25 mg/kg by gavage every 24 hours for three weeks) on the absorption of phenobarbitone, sulphafurazole, isoniazid, mecamylamine and quinidine from the rat small intestine was studied in situ by measuring their disappearance from the intestinal lumen. The appearance of sulphafurazole and mecamylamine in the intestinal lumen was also studied after their intravenous administration, and the partitioning of mecamylamine between the buffer solution and the intestinal tissue was measured in vitro. Treatment with Triparanol retarded the absorption of sulphafurazole, whereas the absorption of mecamylamine was accelerated. The amount of sulphafurazole and mecamylamine in the intestinal lumen after their intravenous administration was relatively slight. The in vitro partitioning of mecamylamine into the intestinal tissue was higher in Triparanol–treated than in control intestines. Triparanol did not change the absorption of phenobarbitone, isoniazid or quinidine. Phenobarbitone in the whole blood at the end of the experiment was increased after Triparanol, but the levels of other drugs were unchanged. Triparanol did not modify drug concentrations in the intestinal wall at the end of the experiment. The relatively slight changes in drug absorption induced by Triparanol are probably due to changes in the morphology and composition of the intestinal wall.

  • Drug Absorption from the Small Intestine of the Triparanol–Treated Rat in Situ
    Pharmacology & Toxicology, 2009
    Co-Authors: V M K Venho
    Abstract:

    The effect of treatment with Triparanol (25 mg/kg by gavage every 24 hours for three weeks) on the absorption of phenobarbitone, sulphafurazole, isoniazid, mecamylamine and quinidine from the rat small intestine was studied in situ by measuring their disappearance from the intestinal lumen. The appearance of sulphafurazole and mecamylamine in the intestinal lumen was also studied after their intravenous administration, and the partitioning of mecamylamine between the buffer solution and the intestinal tissue was measured in vitro. Treatment with Triparanol retarded the absorption of sulphafurazole, whereas the absorption of mecamylamine was accelerated. The amount of sulphafurazole and mecamylamine in the intestinal lumen after their intravenous administration was relatively slight. The in vitro partitioning of mecamylamine into the intestinal tissue was higher in Triparanol–treated than in control intestines. Triparanol did not change the absorption of phenobarbitone, isoniazid or quinidine. Phenobarbitone in the whole blood at the end of the experiment was increased after Triparanol, but the levels of other drugs were unchanged. Triparanol did not modify drug concentrations in the intestinal wall at the end of the experiment. The relatively slight changes in drug absorption induced by Triparanol are probably due to changes in the morphology and composition of the intestinal wall.

Xinyu Bi - One of the best experts on this subject based on the ideXlab platform.

  • Triparanol suppresses human tumor growth in vitro and in vivo
    Biochemical and Biophysical Research Communications, 2012
    Co-Authors: Xinyu Bi, Fang Zhang, Miao He, Yi Zhang, Hong Zhao
    Abstract:

    Highlights: Black-Right-Pointing-Pointer Demonstrate Triparanol can block proliferation in multiple cancer cells. Black-Right-Pointing-Pointer Demonstrate Triparanol can induce apoptosis in multiple cancer cells. Black-Right-Pointing-Pointer Proved Triparanol can inhibit Hedgehog signaling in multiple cancer cells. Black-Right-Pointing-Pointer Demonstrated Triparanol can impede tumor growth in vivo in mouse xenograft model. -- Abstract: Despite the improved contemporary multidisciplinary regimens treating cancer, majority of cancer patients still suffer from adverse effects and relapse, therefore posing a significant challenge to uncover more efficacious molecular therapeutics targeting signaling pathways central to tumorigenesis. Here, our study have demonstrated that Triparanol, a cholesterol synthesis inhibitor, can block proliferation and induce apoptosis in multiple human cancer cells including lung, breast, liver, pancreatic, prostate cancer and melanoma cells, and growth inhibition can be rescued by exogenous addition of cholesterol. Remarkably, we have proved Triparanol can significantly repress Hedgehog pathway signaling in these human cancer cells. Furthermore, study in a mouse xenograft model of human lung cancer has validated that Triparanol can impede tumor growth in vivo. We have therefore uncovered Triparanol as potential new cancer therapeutic in treating multiple types of human cancers with deregulated Hedgehog signaling.

Fang Zhang - One of the best experts on this subject based on the ideXlab platform.

  • Triparanol suppresses human tumor growth in vitro and in vivo
    Biochemical and Biophysical Research Communications, 2012
    Co-Authors: Xinyu Bi, Fang Zhang, Miao He, Yi Zhang, Hong Zhao
    Abstract:

    Highlights: Black-Right-Pointing-Pointer Demonstrate Triparanol can block proliferation in multiple cancer cells. Black-Right-Pointing-Pointer Demonstrate Triparanol can induce apoptosis in multiple cancer cells. Black-Right-Pointing-Pointer Proved Triparanol can inhibit Hedgehog signaling in multiple cancer cells. Black-Right-Pointing-Pointer Demonstrated Triparanol can impede tumor growth in vivo in mouse xenograft model. -- Abstract: Despite the improved contemporary multidisciplinary regimens treating cancer, majority of cancer patients still suffer from adverse effects and relapse, therefore posing a significant challenge to uncover more efficacious molecular therapeutics targeting signaling pathways central to tumorigenesis. Here, our study have demonstrated that Triparanol, a cholesterol synthesis inhibitor, can block proliferation and induce apoptosis in multiple human cancer cells including lung, breast, liver, pancreatic, prostate cancer and melanoma cells, and growth inhibition can be rescued by exogenous addition of cholesterol. Remarkably, we have proved Triparanol can significantly repress Hedgehog pathway signaling in these human cancer cells. Furthermore, study in a mouse xenograft model of human lung cancer has validated that Triparanol can impede tumor growth in vivo. We have therefore uncovered Triparanol as potential new cancer therapeutic in treating multiple types of human cancers with deregulated Hedgehog signaling.

Miao He - One of the best experts on this subject based on the ideXlab platform.

  • Triparanol suppresses human tumor growth in vitro and in vivo
    Biochemical and Biophysical Research Communications, 2012
    Co-Authors: Xinyu Bi, Fang Zhang, Miao He, Yi Zhang, Hong Zhao
    Abstract:

    Highlights: Black-Right-Pointing-Pointer Demonstrate Triparanol can block proliferation in multiple cancer cells. Black-Right-Pointing-Pointer Demonstrate Triparanol can induce apoptosis in multiple cancer cells. Black-Right-Pointing-Pointer Proved Triparanol can inhibit Hedgehog signaling in multiple cancer cells. Black-Right-Pointing-Pointer Demonstrated Triparanol can impede tumor growth in vivo in mouse xenograft model. -- Abstract: Despite the improved contemporary multidisciplinary regimens treating cancer, majority of cancer patients still suffer from adverse effects and relapse, therefore posing a significant challenge to uncover more efficacious molecular therapeutics targeting signaling pathways central to tumorigenesis. Here, our study have demonstrated that Triparanol, a cholesterol synthesis inhibitor, can block proliferation and induce apoptosis in multiple human cancer cells including lung, breast, liver, pancreatic, prostate cancer and melanoma cells, and growth inhibition can be rescued by exogenous addition of cholesterol. Remarkably, we have proved Triparanol can significantly repress Hedgehog pathway signaling in these human cancer cells. Furthermore, study in a mouse xenograft model of human lung cancer has validated that Triparanol can impede tumor growth in vivo. We have therefore uncovered Triparanol as potential new cancer therapeutic in treating multiple types of human cancers with deregulated Hedgehog signaling.