Journal of cancer research and therapeutics · 2018
Cigarette smoke condensate could promote human bronchial epithelial BEAS-2B cell migration through shifting neprilysin trafficking.
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Yang Kun, Zhang Chuanfeng, Sun Lei, Li Dong, Hong Xin
Аннотация
AIM OF STUDY: Recent studies have suggested neprilysin (NEP) play a key role in cigarette smoke-induced nonsmall-cell lung carcinoma; however, the detailed mechanism was still unclear. Here, we employed in vitro human bronchial epithelial BEAS-2B cells to investigate whether and how NEP involved in cigarette smoke condensate (CSC)-induced cancer occurrence.
MATERIALS AND METHODS: In vitro MTT and transwell assay was applied. Live cell imaging and staining were also employed.
RESULTS: In vitro data showed that CSC could increase BEAS-2B cell migration while NEP shRNA could block CSC-induced BEAS-2B cell hypermigration. By biotination and live cell staining, we found that after CSC treatment, cell surface NEP was increased while internalization trafficking was shifted from late endosome/lysosome pathway to recycling pathway. Finally, we found that surface NEP could bind to p120 catenin (p120ctn) for lysosome destination turnover while CSC treatment could change p120ctn membrane/cytosome distribution. Loss of p120ctn will subsequently change NEP trafficking and finally, increase its membrane distribution with a phenocopy manner as CSC.
CONCLUSION: These data indicated under CSC treatment; losing of membrane p120ctn could upregulate surface NEP protein level and thus facilitate BEAS-2B cell migration.
MATERIALS AND METHODS: In vitro MTT and transwell assay was applied. Live cell imaging and staining were also employed.
RESULTS: In vitro data showed that CSC could increase BEAS-2B cell migration while NEP shRNA could block CSC-induced BEAS-2B cell hypermigration. By biotination and live cell staining, we found that after CSC treatment, cell surface NEP was increased while internalization trafficking was shifted from late endosome/lysosome pathway to recycling pathway. Finally, we found that surface NEP could bind to p120 catenin (p120ctn) for lysosome destination turnover while CSC treatment could change p120ctn membrane/cytosome distribution. Loss of p120ctn will subsequently change NEP trafficking and finally, increase its membrane distribution with a phenocopy manner as CSC.
CONCLUSION: These data indicated under CSC treatment; losing of membrane p120ctn could upregulate surface NEP protein level and thus facilitate BEAS-2B cell migration.