Mechanisms of action of nonpeptide hormones on resveratrol-induced antiproliferation of cancer cells

Hung Yun Lin, Meng Ti Hsieh, Guei Yun Cheng, Hsuan Yu Lai, Yu Tang Chin, Ya Jung Shih, André Wendindondé Nana, Shin Ying Lin, Yu Chen S.H. Yang, Heng Yuan Tang, I. Jen Chiang, Kuan Wang

研究成果: 雜誌貢獻回顧型文獻

7 引文 (Scopus)

摘要

Nonpeptide hormones, such as thyroid hormone, dihydrotestosterone, and estrogen, have been shown to stimulate cancer proliferation via different mechanisms. Aside from their cytosolic or membrane-bound receptors, there are receptors on integrin αvβ3 for nonpeptide hormones. Interaction between hormones and integrin αvβ3 can induce signal transduction and eventually stimulate cancer cell proliferation. Resveratrol induces inducible COX-2-dependent antiproliferation via integrin αvβ3. Resveratrol and hormone-induced signals are both transduced by activated extracellular-regulated kinases 1 and 2 (ERK1/2); however, hormones promote cell proliferation, while resveratrol induces antiproliferation in cancer cells. Hormones inhibit resveratrol-stimulated phosphorylation of p53 on Ser15, resveratrol-induced nuclear COX-2 accumulation, and formation of p53-COX-2 nuclear complexes. Subsequently, hormones impair resveratrol-induced COX-2-/p53-dependent gene expression. The inhibitory effects of hormones on resveratrol action can be blocked by different antagonists of specific nonpeptide hormone receptors but not integrin αvβ3 blockers. Results suggest that nonpeptide hormones inhibit resveratrol-induced antiproliferation in cancer cells downstream of the interaction between ligand and receptor and ERK1/2 activation to interfere with nuclear COX-2 accumulation. Thus, the surface receptor sites for resveratrol and nonpeptide hormones are distinct and can induce discrete ERK1/2-dependent downstream antiproliferation biological activities. It also indicates the complex pathways by which antiproliferation is induced by resveratrol in various physiological hormonal environments.
原文英語
頁(從 - 到)92-100
期刊Annals of the New York Academy of Sciences
DOIs
出版狀態接受/付印 - 2017

指紋

Cells
Hormones
Neoplasms
Integrins
Phosphotransferases
Cell proliferation
resveratrol
Cancer
Cell Proliferation
Signal transduction
Phosphorylation
Dihydrotestosterone
p53 Genes
Bioactivity
Thyroid Hormones
Gene expression
Cell Communication
Signal Transduction
Estrogens
Chemical activation

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

引用此文

Mechanisms of action of nonpeptide hormones on resveratrol-induced antiproliferation of cancer cells. / Lin, Hung Yun; Hsieh, Meng Ti; Cheng, Guei Yun; Lai, Hsuan Yu; Chin, Yu Tang; Shih, Ya Jung; Nana, André Wendindondé; Lin, Shin Ying; Yang, Yu Chen S.H.; Tang, Heng Yuan; Chiang, I. Jen; Wang, Kuan.

於: Annals of the New York Academy of Sciences, 2017, p. 92-100.

研究成果: 雜誌貢獻回顧型文獻

Lin, Hung Yun ; Hsieh, Meng Ti ; Cheng, Guei Yun ; Lai, Hsuan Yu ; Chin, Yu Tang ; Shih, Ya Jung ; Nana, André Wendindondé ; Lin, Shin Ying ; Yang, Yu Chen S.H. ; Tang, Heng Yuan ; Chiang, I. Jen ; Wang, Kuan. / Mechanisms of action of nonpeptide hormones on resveratrol-induced antiproliferation of cancer cells. 於: Annals of the New York Academy of Sciences. 2017 ; 頁 92-100.
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title = "Mechanisms of action of nonpeptide hormones on resveratrol-induced antiproliferation of cancer cells",
abstract = "Nonpeptide hormones, such as thyroid hormone, dihydrotestosterone, and estrogen, have been shown to stimulate cancer proliferation via different mechanisms. Aside from their cytosolic or membrane-bound receptors, there are receptors on integrin αvβ3 for nonpeptide hormones. Interaction between hormones and integrin αvβ3 can induce signal transduction and eventually stimulate cancer cell proliferation. Resveratrol induces inducible COX-2-dependent antiproliferation via integrin αvβ3. Resveratrol and hormone-induced signals are both transduced by activated extracellular-regulated kinases 1 and 2 (ERK1/2); however, hormones promote cell proliferation, while resveratrol induces antiproliferation in cancer cells. Hormones inhibit resveratrol-stimulated phosphorylation of p53 on Ser15, resveratrol-induced nuclear COX-2 accumulation, and formation of p53-COX-2 nuclear complexes. Subsequently, hormones impair resveratrol-induced COX-2-/p53-dependent gene expression. The inhibitory effects of hormones on resveratrol action can be blocked by different antagonists of specific nonpeptide hormone receptors but not integrin αvβ3 blockers. Results suggest that nonpeptide hormones inhibit resveratrol-induced antiproliferation in cancer cells downstream of the interaction between ligand and receptor and ERK1/2 activation to interfere with nuclear COX-2 accumulation. Thus, the surface receptor sites for resveratrol and nonpeptide hormones are distinct and can induce discrete ERK1/2-dependent downstream antiproliferation biological activities. It also indicates the complex pathways by which antiproliferation is induced by resveratrol in various physiological hormonal environments.",
keywords = "Apoptosis, ERK1/2 phosphorylation, Nuclear COX-2 accumulation, Resveratrol, Steroid hormones",
author = "Lin, {Hung Yun} and Hsieh, {Meng Ti} and Cheng, {Guei Yun} and Lai, {Hsuan Yu} and Chin, {Yu Tang} and Shih, {Ya Jung} and Nana, {Andr{\'e} Wendindond{\'e}} and Lin, {Shin Ying} and Yang, {Yu Chen S.H.} and Tang, {Heng Yuan} and Chiang, {I. Jen} and Kuan Wang",
year = "2017",
doi = "10.1111/nyas.13423",
language = "English",
pages = "92--100",
journal = "Annals of the New York Academy of Sciences",
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TY - JOUR

T1 - Mechanisms of action of nonpeptide hormones on resveratrol-induced antiproliferation of cancer cells

AU - Lin, Hung Yun

AU - Hsieh, Meng Ti

AU - Cheng, Guei Yun

AU - Lai, Hsuan Yu

AU - Chin, Yu Tang

AU - Shih, Ya Jung

AU - Nana, André Wendindondé

AU - Lin, Shin Ying

AU - Yang, Yu Chen S.H.

AU - Tang, Heng Yuan

AU - Chiang, I. Jen

AU - Wang, Kuan

PY - 2017

Y1 - 2017

N2 - Nonpeptide hormones, such as thyroid hormone, dihydrotestosterone, and estrogen, have been shown to stimulate cancer proliferation via different mechanisms. Aside from their cytosolic or membrane-bound receptors, there are receptors on integrin αvβ3 for nonpeptide hormones. Interaction between hormones and integrin αvβ3 can induce signal transduction and eventually stimulate cancer cell proliferation. Resveratrol induces inducible COX-2-dependent antiproliferation via integrin αvβ3. Resveratrol and hormone-induced signals are both transduced by activated extracellular-regulated kinases 1 and 2 (ERK1/2); however, hormones promote cell proliferation, while resveratrol induces antiproliferation in cancer cells. Hormones inhibit resveratrol-stimulated phosphorylation of p53 on Ser15, resveratrol-induced nuclear COX-2 accumulation, and formation of p53-COX-2 nuclear complexes. Subsequently, hormones impair resveratrol-induced COX-2-/p53-dependent gene expression. The inhibitory effects of hormones on resveratrol action can be blocked by different antagonists of specific nonpeptide hormone receptors but not integrin αvβ3 blockers. Results suggest that nonpeptide hormones inhibit resveratrol-induced antiproliferation in cancer cells downstream of the interaction between ligand and receptor and ERK1/2 activation to interfere with nuclear COX-2 accumulation. Thus, the surface receptor sites for resveratrol and nonpeptide hormones are distinct and can induce discrete ERK1/2-dependent downstream antiproliferation biological activities. It also indicates the complex pathways by which antiproliferation is induced by resveratrol in various physiological hormonal environments.

AB - Nonpeptide hormones, such as thyroid hormone, dihydrotestosterone, and estrogen, have been shown to stimulate cancer proliferation via different mechanisms. Aside from their cytosolic or membrane-bound receptors, there are receptors on integrin αvβ3 for nonpeptide hormones. Interaction between hormones and integrin αvβ3 can induce signal transduction and eventually stimulate cancer cell proliferation. Resveratrol induces inducible COX-2-dependent antiproliferation via integrin αvβ3. Resveratrol and hormone-induced signals are both transduced by activated extracellular-regulated kinases 1 and 2 (ERK1/2); however, hormones promote cell proliferation, while resveratrol induces antiproliferation in cancer cells. Hormones inhibit resveratrol-stimulated phosphorylation of p53 on Ser15, resveratrol-induced nuclear COX-2 accumulation, and formation of p53-COX-2 nuclear complexes. Subsequently, hormones impair resveratrol-induced COX-2-/p53-dependent gene expression. The inhibitory effects of hormones on resveratrol action can be blocked by different antagonists of specific nonpeptide hormone receptors but not integrin αvβ3 blockers. Results suggest that nonpeptide hormones inhibit resveratrol-induced antiproliferation in cancer cells downstream of the interaction between ligand and receptor and ERK1/2 activation to interfere with nuclear COX-2 accumulation. Thus, the surface receptor sites for resveratrol and nonpeptide hormones are distinct and can induce discrete ERK1/2-dependent downstream antiproliferation biological activities. It also indicates the complex pathways by which antiproliferation is induced by resveratrol in various physiological hormonal environments.

KW - Apoptosis

KW - ERK1/2 phosphorylation

KW - Nuclear COX-2 accumulation

KW - Resveratrol

KW - Steroid hormones

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U2 - 10.1111/nyas.13423

DO - 10.1111/nyas.13423

M3 - Review article

SP - 92

EP - 100

JO - Annals of the New York Academy of Sciences

JF - Annals of the New York Academy of Sciences

SN - 0077-8923

ER -