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Article: Myeloid-derived suppressor cells promote lung cancer metastasis by CCL11 to activate ERK and AKT signaling and induce epithelial-mesenchymal transition in tumor cells

TitleMyeloid-derived suppressor cells promote lung cancer metastasis by CCL11 to activate ERK and AKT signaling and induce epithelial-mesenchymal transition in tumor cells
Authors
Issue Date2021
PublisherSpringer Nature [academic journals on nature.com]: Hybrid Journal. The Journal's web site is located at http://www.nature.com/onc
Citation
Oncogene, 2021, v. 40, p. 1476-1489 How to Cite?
AbstractMyeloid-derived suppressor cells (MDSCs) suppress antitumor immune activities and facilitate cancer progression. Although the concept of immunosuppressive MDSCs is well established, the mechanism that MDSCs regulate non-small cell lung cancer (NSCLC) progression through the paracrine signals is still lacking. Here, we reported that the infiltration of MDSCs within NSCLC tissues was associated with the progression of cancer status, and was positively correlated with the Patient-derived xenograft model establishment, and poor patient prognosis. Intratumoral MDSCs directly promoted NSCLC metastasis and highly expressed chemokines that promote NSCLC cells invasion, including CCL11. CCL11 was capable of activating the AKT and ERK signaling pathways to promote NSCLC metastasis through the epithelial-mesenchymal transition (EMT) process. Moreover, high expression of CCL11 was associated with a poor prognosis in lung cancer as well as other types of cancer. Our findings underscore that MDSCs produce CCL11 to promote NSCLC metastasis via activation of ERK and AKT signaling and induction of EMT, suggesting that the MDSCs-CCL11-ERK/AKT-EMT axis contains potential targets for NSCLC metastasis treatment.
Persistent Identifierhttp://hdl.handle.net/10722/295765
ISSN
2020 Impact Factor: 9.867
2015 SCImago Journal Rankings: 4.047
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLin, S-
dc.contributor.authorZhang, X-
dc.contributor.authorHuang, G-
dc.contributor.authorCheng, L-
dc.contributor.authorLv, J-
dc.contributor.authorZheng, D-
dc.contributor.authorLin, S-
dc.contributor.authorWang, S-
dc.contributor.authorWu, Q-
dc.contributor.authorLong, Y-
dc.contributor.authorLi, B-
dc.contributor.authorWei, W-
dc.contributor.authorLiu, P-
dc.contributor.authorPei, D-
dc.contributor.authorLi, Y-
dc.contributor.authorWen, Z-
dc.contributor.authorCui, S-
dc.contributor.authorLi, P-
dc.contributor.authorSun, X-
dc.contributor.authorWu, Y-
dc.contributor.authorYao, Y-
dc.date.accessioned2021-02-08T08:13:41Z-
dc.date.available2021-02-08T08:13:41Z-
dc.date.issued2021-
dc.identifier.citationOncogene, 2021, v. 40, p. 1476-1489-
dc.identifier.issn0950-9232-
dc.identifier.urihttp://hdl.handle.net/10722/295765-
dc.description.abstractMyeloid-derived suppressor cells (MDSCs) suppress antitumor immune activities and facilitate cancer progression. Although the concept of immunosuppressive MDSCs is well established, the mechanism that MDSCs regulate non-small cell lung cancer (NSCLC) progression through the paracrine signals is still lacking. Here, we reported that the infiltration of MDSCs within NSCLC tissues was associated with the progression of cancer status, and was positively correlated with the Patient-derived xenograft model establishment, and poor patient prognosis. Intratumoral MDSCs directly promoted NSCLC metastasis and highly expressed chemokines that promote NSCLC cells invasion, including CCL11. CCL11 was capable of activating the AKT and ERK signaling pathways to promote NSCLC metastasis through the epithelial-mesenchymal transition (EMT) process. Moreover, high expression of CCL11 was associated with a poor prognosis in lung cancer as well as other types of cancer. Our findings underscore that MDSCs produce CCL11 to promote NSCLC metastasis via activation of ERK and AKT signaling and induction of EMT, suggesting that the MDSCs-CCL11-ERK/AKT-EMT axis contains potential targets for NSCLC metastasis treatment.-
dc.languageeng-
dc.publisherSpringer Nature [academic journals on nature.com]: Hybrid Journal. The Journal's web site is located at http://www.nature.com/onc-
dc.relation.ispartofOncogene-
dc.titleMyeloid-derived suppressor cells promote lung cancer metastasis by CCL11 to activate ERK and AKT signaling and induce epithelial-mesenchymal transition in tumor cells-
dc.typeArticle-
dc.identifier.emailLiu, P: pliu88@hku.hk-
dc.identifier.authorityLiu, P=rp02328-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/s41388-020-01605-4-
dc.identifier.pmid33452453-
dc.identifier.hkuros321208-
dc.identifier.volume40-
dc.identifier.spage1476-
dc.identifier.epage1489-
dc.identifier.isiWOS:000607998600011-
dc.publisher.placeUnited Kingdom-

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