Integrin-Mediated Actions of Thyroid Hormone Analogues on Tumor Cell Chemosensitivity, Integrin-Growth Factor Receptor Crosstalk and Inflammatory Gene Expression.

Aleck Hercbergs, Faith B. Davis, Hung-Yun Lin, Mary K. Luidens, Ran Meng, Osnat Ashur-Fabian, Shaker A. Mousa, Paul J. Davis

Research output: Contribution to journalArticle

Abstract

Tetraiodothyroacetic acid (tetrac) and its nanoparticulate formulation induce apoptosis in cancer cells, oppose angiogenesis about xenografted human tumors and block cancer cell repair of double-stranded DNA breaks. These nongenomic actions of tetrac are initiated at a tetrac-thyroid hormone receptor on plasma membrane integrin avb3. In this review, we examine additional anti-cancer activities of tetrac formulations at avb3 and what is known about their mechanisms. These activities include 1) reversal of cancer cell chemoresistance (= induction of chemosensitization) and 2) disruption of crosstalk between avb3 and nearby cell surface growth factor receptors. In addition, nanoparticulate tetrac 3) alters expression of differentially-regulated inflammation-relevant genes that may be important to inflammation-supported cancer. For example, the agent downregulates genes whose products mediate cytokine responses and upregulates suppressor of cytokine signaling, SOCS4. Such actions of tetrac formulations define a multi-target functional profile, although the activities of tetrac begin at a single anatomic plasma membrane receptor on integrin avb3.
Original languageEnglish
Pages (from-to)32-40
Number of pages9
JournalCancer and Clinical Oncology
Volume1
Publication statusPublished - 2012

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Growth Factor Receptors
Thyroid Hormones
Integrins
Gene Expression
Neoplasms
Cell Membrane
Cytokines
Inflammation
Thyroid Hormone Receptors
Double-Stranded DNA Breaks
tetraiodothyroacetic acid
Genes
Up-Regulation
Down-Regulation
Apoptosis

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Integrin-Mediated Actions of Thyroid Hormone Analogues on Tumor Cell Chemosensitivity, Integrin-Growth Factor Receptor Crosstalk and Inflammatory Gene Expression. / Hercbergs, Aleck; Davis, Faith B.; Lin, Hung-Yun; Luidens, Mary K.; Meng, Ran; Ashur-Fabian, Osnat; Mousa, Shaker A.; Davis, Paul J.

In: Cancer and Clinical Oncology , Vol. 1, 2012, p. 32-40.

Research output: Contribution to journalArticle

Hercbergs, Aleck ; Davis, Faith B. ; Lin, Hung-Yun ; Luidens, Mary K. ; Meng, Ran ; Ashur-Fabian, Osnat ; Mousa, Shaker A. ; Davis, Paul J. / Integrin-Mediated Actions of Thyroid Hormone Analogues on Tumor Cell Chemosensitivity, Integrin-Growth Factor Receptor Crosstalk and Inflammatory Gene Expression. In: Cancer and Clinical Oncology . 2012 ; Vol. 1. pp. 32-40.
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abstract = "Tetraiodothyroacetic acid (tetrac) and its nanoparticulate formulation induce apoptosis in cancer cells, oppose angiogenesis about xenografted human tumors and block cancer cell repair of double-stranded DNA breaks. These nongenomic actions of tetrac are initiated at a tetrac-thyroid hormone receptor on plasma membrane integrin avb3. In this review, we examine additional anti-cancer activities of tetrac formulations at avb3 and what is known about their mechanisms. These activities include 1) reversal of cancer cell chemoresistance (= induction of chemosensitization) and 2) disruption of crosstalk between avb3 and nearby cell surface growth factor receptors. In addition, nanoparticulate tetrac 3) alters expression of differentially-regulated inflammation-relevant genes that may be important to inflammation-supported cancer. For example, the agent downregulates genes whose products mediate cytokine responses and upregulates suppressor of cytokine signaling, SOCS4. Such actions of tetrac formulations define a multi-target functional profile, although the activities of tetrac begin at a single anatomic plasma membrane receptor on integrin avb3.",
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AB - Tetraiodothyroacetic acid (tetrac) and its nanoparticulate formulation induce apoptosis in cancer cells, oppose angiogenesis about xenografted human tumors and block cancer cell repair of double-stranded DNA breaks. These nongenomic actions of tetrac are initiated at a tetrac-thyroid hormone receptor on plasma membrane integrin avb3. In this review, we examine additional anti-cancer activities of tetrac formulations at avb3 and what is known about their mechanisms. These activities include 1) reversal of cancer cell chemoresistance (= induction of chemosensitization) and 2) disruption of crosstalk between avb3 and nearby cell surface growth factor receptors. In addition, nanoparticulate tetrac 3) alters expression of differentially-regulated inflammation-relevant genes that may be important to inflammation-supported cancer. For example, the agent downregulates genes whose products mediate cytokine responses and upregulates suppressor of cytokine signaling, SOCS4. Such actions of tetrac formulations define a multi-target functional profile, although the activities of tetrac begin at a single anatomic plasma membrane receptor on integrin avb3.

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