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Oncotarget ; 7(21): 31243-56, 2016 May 24.
Artigo em Inglês | MEDLINE | ID: mdl-27145282

RESUMO

We reported previously that human fibroblasts release 5-methoxytryptophan (5-MTP) which inhibits cancer cell COX-2 overexpression and suppresses cancer cell migration and metastasis. To determine whether fibroblasts block cancer cell epithelial mesenchymal transition (EMT) via 5-MTP, we evaluated the effect of Hs68 fibroblasts (HsFb) on A549 cancer cell EMT in a two-chamber system. Co-incubation of A549 with HsFb prevented TGF-ß1-induced reduction of E-cadherin and increase in Snail and N-cadherin. Transfection of HsFb with tryptophan hydroxylase-1 siRNA, which inhibited tryptophan hydroxylase-1 protein expression and 5-MTP release in HsFb abrogated the effect of HsFb on A549 EMT. Direct addition of pure 5-MTP to cultured A549 cells followed by TGF-ß1 prevented TGF-ß1-induced reduction of E-cadherin, and elevation of Snail, vimentin and matrix metalloproteinase 9. Administration of 5-MTP to a murine xenograft tumor model reduced vimentin protein expression in the tumor tissues compared to vehicle control which was correlated with reduction of metastasis in the 5-MTP treated mice. Our experimental data suggest that 5-MTP exerted its anti-EMT actions through inhibition of p38 MAPK activation, p65/p50 NF-κB nuclear translocation and transactivation without the involvement of COX-2 or p300 histone acetyltransferase. Our findings indicate that fibroblasts release a tryptophan metabolite, 5-MTP, to reduce cancer cell EMT, migration, invasion and metastasis.


Assuntos
Transição Epitelial-Mesenquimal/efeitos dos fármacos , Fibroblastos/metabolismo , Neoplasias Pulmonares/tratamento farmacológico , Triptofano/análogos & derivados , Ensaios Antitumorais Modelo de Xenoenxerto , Células A549 , Animais , Caderinas/metabolismo , Linhagem Celular , Técnicas de Cocultura/métodos , Fibroblastos/citologia , Humanos , Neoplasias Pulmonares/metabolismo , Neoplasias Pulmonares/patologia , Camundongos SCID , NF-kappa B/metabolismo , Interferência de RNA , Fator de Crescimento Transformador beta1/farmacologia , Triptofano/metabolismo , Triptofano/farmacologia , Triptofano Hidroxilase/genética , Triptofano Hidroxilase/metabolismo , Vimentina/metabolismo , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
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