Exosomes derived from -treated lung cancer cells promote the growth of lung cancer via the Wnt3a/-catenin pathway
Fine particulate matter (P[M.sub.2.5]) is associated with an increased lung cancer risk. However, the effect of P[M.sub.2.5] exposure on lung cancer cells is still largely unknown. The present study revealed that A549 lung cancer cells secreted exosomes containing high levels of Wnt3a after treatmen...
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Veröffentlicht in: | Oncology reports 2019-02, Vol.41 (2), p.1180 |
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description | Fine particulate matter (P[M.sub.2.5]) is associated with an increased lung cancer risk. However, the effect of P[M.sub.2.5] exposure on lung cancer cells is still largely unknown. The present study revealed that A549 lung cancer cells secreted exosomes containing high levels of Wnt3a after treatment with P[M.sub.2.5]. These exosomes activated [beta]-catenin signalling in A549 cells. These exosomes exhibited no effects on migration and invasion, but promoted proliferation of A549 cells via the Wnt3a/[beta]-catenin pathway in vitro. These exosomes promoted A549 tumour progression in a Wnt3a-dependent fashion in vivo. These results demonstrated that P[M.sub.2.5] has a direct effect on promoting lung tumour development. Inhibition of exosome production by tumour cells or blockade of the Wnt3a/[beta]-catenin pathway represents a promising strategy to impede P[M.sub.2.5]-mediated lung tumour progression. |
doi_str_mv | 10.3892/or.2018.6862 |
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However, the effect of P[M.sub.2.5] exposure on lung cancer cells is still largely unknown. The present study revealed that A549 lung cancer cells secreted exosomes containing high levels of Wnt3a after treatment with P[M.sub.2.5]. These exosomes activated [beta]-catenin signalling in A549 cells. These exosomes exhibited no effects on migration and invasion, but promoted proliferation of A549 cells via the Wnt3a/[beta]-catenin pathway in vitro. These exosomes promoted A549 tumour progression in a Wnt3a-dependent fashion in vivo. These results demonstrated that P[M.sub.2.5] has a direct effect on promoting lung tumour development. Inhibition of exosome production by tumour cells or blockade of the Wnt3a/[beta]-catenin pathway represents a promising strategy to impede P[M.sub.2.5]-mediated lung tumour progression.</description><identifier>ISSN: 1021-335X</identifier><identifier>DOI: 10.3892/or.2018.6862</identifier><language>eng</language><publisher>Spandidos Publications</publisher><subject>Care and treatment ; Cellular signal transduction ; Development and progression ; Health aspects ; Lung cancer ; Particulate matter</subject><ispartof>Oncology reports, 2019-02, Vol.41 (2), p.1180</ispartof><rights>COPYRIGHT 2019 Spandidos Publications</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>Xu, Hui</creatorcontrib><creatorcontrib>Jiao, Xingai</creatorcontrib><creatorcontrib>Wu, Yilei</creatorcontrib><creatorcontrib>Li, Shuo</creatorcontrib><creatorcontrib>Cao, Lili</creatorcontrib><creatorcontrib>Dong, Liang</creatorcontrib><title>Exosomes derived from -treated lung cancer cells promote the growth of lung cancer via the Wnt3a/-catenin pathway</title><title>Oncology reports</title><description>Fine particulate matter (P[M.sub.2.5]) is associated with an increased lung cancer risk. However, the effect of P[M.sub.2.5] exposure on lung cancer cells is still largely unknown. The present study revealed that A549 lung cancer cells secreted exosomes containing high levels of Wnt3a after treatment with P[M.sub.2.5]. These exosomes activated [beta]-catenin signalling in A549 cells. These exosomes exhibited no effects on migration and invasion, but promoted proliferation of A549 cells via the Wnt3a/[beta]-catenin pathway in vitro. These exosomes promoted A549 tumour progression in a Wnt3a-dependent fashion in vivo. These results demonstrated that P[M.sub.2.5] has a direct effect on promoting lung tumour development. 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However, the effect of P[M.sub.2.5] exposure on lung cancer cells is still largely unknown. The present study revealed that A549 lung cancer cells secreted exosomes containing high levels of Wnt3a after treatment with P[M.sub.2.5]. These exosomes activated [beta]-catenin signalling in A549 cells. These exosomes exhibited no effects on migration and invasion, but promoted proliferation of A549 cells via the Wnt3a/[beta]-catenin pathway in vitro. These exosomes promoted A549 tumour progression in a Wnt3a-dependent fashion in vivo. These results demonstrated that P[M.sub.2.5] has a direct effect on promoting lung tumour development. Inhibition of exosome production by tumour cells or blockade of the Wnt3a/[beta]-catenin pathway represents a promising strategy to impede P[M.sub.2.5]-mediated lung tumour progression.</abstract><pub>Spandidos Publications</pub><doi>10.3892/or.2018.6862</doi></addata></record> |
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subjects | Care and treatment Cellular signal transduction Development and progression Health aspects Lung cancer Particulate matter |
title | Exosomes derived from -treated lung cancer cells promote the growth of lung cancer via the Wnt3a/-catenin pathway |
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