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Lycopene Inhibits Epithelial–Mesenchymal Transition and Promotes Apoptosis in Oral Cancer via PI3K/AKT/m-TOR Signal Pathway
BACKGROUND: Oral cancer (OC) is one of the most common cancers around the world. Despite the progress in treatment, the prognosis of OC remains poor, especially for patients with advanced diseases. It urges the development of novel therapeutic options against OC. Lycopene (LYC) is an antioxidant wit...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7321693/ https://www.ncbi.nlm.nih.gov/pubmed/32606612 http://dx.doi.org/10.2147/DDDT.S251614 |
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author | Wang, Ran Lu, Xinxing Yu, Riyue |
author_facet | Wang, Ran Lu, Xinxing Yu, Riyue |
author_sort | Wang, Ran |
collection | PubMed |
description | BACKGROUND: Oral cancer (OC) is one of the most common cancers around the world. Despite the progress in treatment, the prognosis of OC remains poor, especially for patients with advanced diseases. It urges the development of novel therapeutic options against OC. Lycopene (LYC) is an antioxidant with chemoprotective properties against cancer. However, little is known about the mechanisms underlying the protective role of LYC in OC tumorigenesis. METHODS: In this study, we investigated the anti-cancer effect of LYC on the progression of OC in vitro and in vivo and explored the underlying mechanisms involved in this process. RESULTS: LYC inhibited OC cell proliferation, migration, invasion, apoptosis, and xenograft tumor growth in a dose-dependent manner. Furthermore, we found that LYC might inhibit epithelial–mesenchymal transition and induce apoptosis in OC cells by deactivating the PI3K/AKT/m-TOR signaling through increasing the levels of E-cadherin and Bax and downregulating N-cadherin, p-PI3K, p-AKT, p-m-TOR, and bcl-2. CONCLUSION: We reported for the first time that LYC exhibited anti-cancer effects on OC development both in vitro and in vivo via regulating EMT process and apoptosis. These findings provide support for the potential clinical use of LYC in OC treatment. |
format | Online Article Text |
id | pubmed-7321693 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-73216932020-06-29 Lycopene Inhibits Epithelial–Mesenchymal Transition and Promotes Apoptosis in Oral Cancer via PI3K/AKT/m-TOR Signal Pathway Wang, Ran Lu, Xinxing Yu, Riyue Drug Des Devel Ther Original Research BACKGROUND: Oral cancer (OC) is one of the most common cancers around the world. Despite the progress in treatment, the prognosis of OC remains poor, especially for patients with advanced diseases. It urges the development of novel therapeutic options against OC. Lycopene (LYC) is an antioxidant with chemoprotective properties against cancer. However, little is known about the mechanisms underlying the protective role of LYC in OC tumorigenesis. METHODS: In this study, we investigated the anti-cancer effect of LYC on the progression of OC in vitro and in vivo and explored the underlying mechanisms involved in this process. RESULTS: LYC inhibited OC cell proliferation, migration, invasion, apoptosis, and xenograft tumor growth in a dose-dependent manner. Furthermore, we found that LYC might inhibit epithelial–mesenchymal transition and induce apoptosis in OC cells by deactivating the PI3K/AKT/m-TOR signaling through increasing the levels of E-cadherin and Bax and downregulating N-cadherin, p-PI3K, p-AKT, p-m-TOR, and bcl-2. CONCLUSION: We reported for the first time that LYC exhibited anti-cancer effects on OC development both in vitro and in vivo via regulating EMT process and apoptosis. These findings provide support for the potential clinical use of LYC in OC treatment. Dove 2020-06-24 /pmc/articles/PMC7321693/ /pubmed/32606612 http://dx.doi.org/10.2147/DDDT.S251614 Text en © 2020 Wang et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Wang, Ran Lu, Xinxing Yu, Riyue Lycopene Inhibits Epithelial–Mesenchymal Transition and Promotes Apoptosis in Oral Cancer via PI3K/AKT/m-TOR Signal Pathway |
title | Lycopene Inhibits Epithelial–Mesenchymal Transition and Promotes Apoptosis in Oral Cancer via PI3K/AKT/m-TOR Signal Pathway |
title_full | Lycopene Inhibits Epithelial–Mesenchymal Transition and Promotes Apoptosis in Oral Cancer via PI3K/AKT/m-TOR Signal Pathway |
title_fullStr | Lycopene Inhibits Epithelial–Mesenchymal Transition and Promotes Apoptosis in Oral Cancer via PI3K/AKT/m-TOR Signal Pathway |
title_full_unstemmed | Lycopene Inhibits Epithelial–Mesenchymal Transition and Promotes Apoptosis in Oral Cancer via PI3K/AKT/m-TOR Signal Pathway |
title_short | Lycopene Inhibits Epithelial–Mesenchymal Transition and Promotes Apoptosis in Oral Cancer via PI3K/AKT/m-TOR Signal Pathway |
title_sort | lycopene inhibits epithelial–mesenchymal transition and promotes apoptosis in oral cancer via pi3k/akt/m-tor signal pathway |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7321693/ https://www.ncbi.nlm.nih.gov/pubmed/32606612 http://dx.doi.org/10.2147/DDDT.S251614 |
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