Triclosan potentiates epithelial-to-mesenchymal transition in anoikis-resistant human lung cancer cells.

Alteration of cancer cell toward mesenchymal phenotype has been shown to potentiate tumor aggressiveness by increasing cancer cell metastasis. Herein, we report the effect of triclosan, a widely used antibacterial agent found in many daily products, in enhancing the epithelial-to-mesenchymal transit...

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Autores principales: Thidarat Winitthana, Somsong Lawanprasert, Pithi Chanvorachote
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Lenguaje:EN
Publicado: Public Library of Science (PLoS) 2014
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Acceso en línea:https://doaj.org/article/4619814547c542fcb0ba6e90225e6f2e
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spelling oai:doaj.org-article:4619814547c542fcb0ba6e90225e6f2e2021-11-25T05:56:22ZTriclosan potentiates epithelial-to-mesenchymal transition in anoikis-resistant human lung cancer cells.1932-620310.1371/journal.pone.0110851https://doaj.org/article/4619814547c542fcb0ba6e90225e6f2e2014-01-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0110851https://doaj.org/toc/1932-6203Alteration of cancer cell toward mesenchymal phenotype has been shown to potentiate tumor aggressiveness by increasing cancer cell metastasis. Herein, we report the effect of triclosan, a widely used antibacterial agent found in many daily products, in enhancing the epithelial-to-mesenchymal transition (EMT) in aggressive anoikis resistant human H460 lung cancer cells. EMT has been long known to increase abilities of the cells to increase migration, invasion, and survival in circulating system. The present study reveals that treatment of the cancer cells with triclosan at the physiologically related concentrations significantly increased the colony number of the cancer cells assessed by tumor formation assay. Also, the mesenchymal-like morphology and decrease in cell-to-cell adhesion were observed in triclosan-treated cells. Importantly, western blot analysis revealed that triclosan-treated cells exhibited decreased E-cadherin, while the levels of EMT markers, namely N-cadherin, vimentin, snail and slug were found to be significantly up-regulated. Furthermore, EMT induced by triclosan treatment was accompanied by the activation of focal adhesion kinase/ATP dependent tyrosine kinase (FAK/Akt) and Ras-related C3 botulinum toxin substrate 1 (Rac1), which enhanced the ability of the cells to migrate and invade. In conclusion, we demonstrated for the first time that triclosan may potentiate cancer cells survival in detached condition and motility via the process of EMT. As mentioned capabilities are required for success in metastasis, the present study provides the novel toxicological information and encourages the awareness of triclosan use in cancer patients.Thidarat WinitthanaSomsong LawanprasertPithi ChanvorachotePublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 10, p e110851 (2014)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Thidarat Winitthana
Somsong Lawanprasert
Pithi Chanvorachote
Triclosan potentiates epithelial-to-mesenchymal transition in anoikis-resistant human lung cancer cells.
description Alteration of cancer cell toward mesenchymal phenotype has been shown to potentiate tumor aggressiveness by increasing cancer cell metastasis. Herein, we report the effect of triclosan, a widely used antibacterial agent found in many daily products, in enhancing the epithelial-to-mesenchymal transition (EMT) in aggressive anoikis resistant human H460 lung cancer cells. EMT has been long known to increase abilities of the cells to increase migration, invasion, and survival in circulating system. The present study reveals that treatment of the cancer cells with triclosan at the physiologically related concentrations significantly increased the colony number of the cancer cells assessed by tumor formation assay. Also, the mesenchymal-like morphology and decrease in cell-to-cell adhesion were observed in triclosan-treated cells. Importantly, western blot analysis revealed that triclosan-treated cells exhibited decreased E-cadherin, while the levels of EMT markers, namely N-cadherin, vimentin, snail and slug were found to be significantly up-regulated. Furthermore, EMT induced by triclosan treatment was accompanied by the activation of focal adhesion kinase/ATP dependent tyrosine kinase (FAK/Akt) and Ras-related C3 botulinum toxin substrate 1 (Rac1), which enhanced the ability of the cells to migrate and invade. In conclusion, we demonstrated for the first time that triclosan may potentiate cancer cells survival in detached condition and motility via the process of EMT. As mentioned capabilities are required for success in metastasis, the present study provides the novel toxicological information and encourages the awareness of triclosan use in cancer patients.
format article
author Thidarat Winitthana
Somsong Lawanprasert
Pithi Chanvorachote
author_facet Thidarat Winitthana
Somsong Lawanprasert
Pithi Chanvorachote
author_sort Thidarat Winitthana
title Triclosan potentiates epithelial-to-mesenchymal transition in anoikis-resistant human lung cancer cells.
title_short Triclosan potentiates epithelial-to-mesenchymal transition in anoikis-resistant human lung cancer cells.
title_full Triclosan potentiates epithelial-to-mesenchymal transition in anoikis-resistant human lung cancer cells.
title_fullStr Triclosan potentiates epithelial-to-mesenchymal transition in anoikis-resistant human lung cancer cells.
title_full_unstemmed Triclosan potentiates epithelial-to-mesenchymal transition in anoikis-resistant human lung cancer cells.
title_sort triclosan potentiates epithelial-to-mesenchymal transition in anoikis-resistant human lung cancer cells.
publisher Public Library of Science (PLoS)
publishDate 2014
url https://doaj.org/article/4619814547c542fcb0ba6e90225e6f2e
work_keys_str_mv AT thidaratwinitthana triclosanpotentiatesepithelialtomesenchymaltransitioninanoikisresistanthumanlungcancercells
AT somsonglawanprasert triclosanpotentiatesepithelialtomesenchymaltransitioninanoikisresistanthumanlungcancercells
AT pithichanvorachote triclosanpotentiatesepithelialtomesenchymaltransitioninanoikisresistanthumanlungcancercells
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