Mechanism of metastasis suppression by luteolin in breast cancer

Matthew T Cook Department of Biology, Washburn University, Topeka, KS, USA Abstract: Metastatic breast cancer is typically an extremely aggressive cancer with poor prognosis. Metastasis requires the orchestration of homeostatic factors and cellular programs, many of which are potential therapeutic t...

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Autor principal: Cook MT
Formato: article
Lenguaje:EN
Publicado: Dove Medical Press 2018
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RTK
AKT
Acceso en línea:https://doaj.org/article/b1616cfbccc14ac4993b8c385421598c
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spelling oai:doaj.org-article:b1616cfbccc14ac4993b8c385421598c2021-12-02T01:17:18ZMechanism of metastasis suppression by luteolin in breast cancer1179-1314https://doaj.org/article/b1616cfbccc14ac4993b8c385421598c2018-06-01T00:00:00Zhttps://www.dovepress.com/mechanism-of-metastasis-suppression-by-luteolin-in-breast-cancer-peer-reviewed-article-BCTThttps://doaj.org/toc/1179-1314Matthew T Cook Department of Biology, Washburn University, Topeka, KS, USA Abstract: Metastatic breast cancer is typically an extremely aggressive cancer with poor prognosis. Metastasis requires the orchestration of homeostatic factors and cellular programs, many of which are potential therapeutic targets. Luteolin (2-[3,4-dihydroxyphenyl]-5,7-dihydroxy-4-chromenone), is a naturally occurring flavonoid found in fruits and vegetables that exhibits many anticancer properties. Luteolin obstructs metastasis through both direct and indirect mechanisms. For instance, luteolin may suppress breast cancer invasion by acting as an antiangiogenic therapeutic inhibiting VEGF production and its receptor’s activity. Furthermore, luteolin decreases epithelial–mesenchymal transition markers and metastatic proclivity. Luteolin also acts as an antiproliferative by suppressing receptor tyrosine-kinase activity and apoptosis, both of which could prevent incipient colonization of breast cancer. Many of these antimetastatic characteristics accredited to luteolin are likely functionally related. For instance, the PI3K/Akt pathway, which is impeded by luteolin, has several downstream programs involved in increased proliferation, survival, and metastatic potential in breast cancer. In this review, luteolin’s ability to ameliorate breast cancer is summarized. The paper also offers insight into the molecular mechanisms by which luteolin may suppress breast cancer metastasis. Keywords: angiogenesis, MMP, NOTCH, β-catenin, RTK, AktCook MTDove Medical PressarticleluteolinmetastasisNOTCHβ-cateninRTKAKTNeoplasms. Tumors. Oncology. Including cancer and carcinogensRC254-282ENBreast Cancer: Targets and Therapy, Vol Volume 10, Pp 89-100 (2018)
institution DOAJ
collection DOAJ
language EN
topic luteolin
metastasis
NOTCH
β-catenin
RTK
AKT
Neoplasms. Tumors. Oncology. Including cancer and carcinogens
RC254-282
spellingShingle luteolin
metastasis
NOTCH
β-catenin
RTK
AKT
Neoplasms. Tumors. Oncology. Including cancer and carcinogens
RC254-282
Cook MT
Mechanism of metastasis suppression by luteolin in breast cancer
description Matthew T Cook Department of Biology, Washburn University, Topeka, KS, USA Abstract: Metastatic breast cancer is typically an extremely aggressive cancer with poor prognosis. Metastasis requires the orchestration of homeostatic factors and cellular programs, many of which are potential therapeutic targets. Luteolin (2-[3,4-dihydroxyphenyl]-5,7-dihydroxy-4-chromenone), is a naturally occurring flavonoid found in fruits and vegetables that exhibits many anticancer properties. Luteolin obstructs metastasis through both direct and indirect mechanisms. For instance, luteolin may suppress breast cancer invasion by acting as an antiangiogenic therapeutic inhibiting VEGF production and its receptor’s activity. Furthermore, luteolin decreases epithelial–mesenchymal transition markers and metastatic proclivity. Luteolin also acts as an antiproliferative by suppressing receptor tyrosine-kinase activity and apoptosis, both of which could prevent incipient colonization of breast cancer. Many of these antimetastatic characteristics accredited to luteolin are likely functionally related. For instance, the PI3K/Akt pathway, which is impeded by luteolin, has several downstream programs involved in increased proliferation, survival, and metastatic potential in breast cancer. In this review, luteolin’s ability to ameliorate breast cancer is summarized. The paper also offers insight into the molecular mechanisms by which luteolin may suppress breast cancer metastasis. Keywords: angiogenesis, MMP, NOTCH, β-catenin, RTK, Akt
format article
author Cook MT
author_facet Cook MT
author_sort Cook MT
title Mechanism of metastasis suppression by luteolin in breast cancer
title_short Mechanism of metastasis suppression by luteolin in breast cancer
title_full Mechanism of metastasis suppression by luteolin in breast cancer
title_fullStr Mechanism of metastasis suppression by luteolin in breast cancer
title_full_unstemmed Mechanism of metastasis suppression by luteolin in breast cancer
title_sort mechanism of metastasis suppression by luteolin in breast cancer
publisher Dove Medical Press
publishDate 2018
url https://doaj.org/article/b1616cfbccc14ac4993b8c385421598c
work_keys_str_mv AT cookmt mechanismofmetastasissuppressionbyluteolininbreastcancer
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