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Article: CHL1 suppresses tumor growth and metastasis in nasopharyngeal carcinoma by repressing PI3K/AKT signaling pathway via interaction with Integrin β1 and Merlin

TitleCHL1 suppresses tumor growth and metastasis in nasopharyngeal carcinoma by repressing PI3K/AKT signaling pathway via interaction with Integrin β1 and Merlin
Authors
Keywordsnasopharyngeal carcinoma
tumor suppressor gene
tumor invasion
tumor metastasis
Issue Date2019
PublisherIvyspring International Publisher. The Journal's web site is located at http://www.biolsci.org/index.htm
Citation
International Journal of Biological Sciences, 2019, v. 15 n. 9, p. 1802-1815 How to Cite?
AbstractDeletion of Chromosome 3p is one of the most frequently detected genetic alterations in nasopharyngeal carcinoma (NPC). We reported the role of a novel 3p26.3 tumor suppressor gene (TSG) CHL1 in NPC. Down-regulation of CHL1 was detected in 4/6 of NPC cell lines and 71/95 (74.7%) in clinical tissues. Ectopic expressions of CHL1 in NPC cells significantly inhibit colony formation and cell motility in functional study. By up-regulating epithelial markers and down-regulating mesenchymal markers CHL1 could induce mesenchymal-epithelial transition (MET), a key step in preventing tumor invasion and metastasis. CHL1 could also cause the inactivation of RhoA/Rac1/Cdc42 signaling pathway and inhibit the formation of stress fiber, lamellipodia, and filopodia. CHL1 could co-localize with adhesion molecule Integrin-β1, the expression of CHL1 was positively correlated with Integrin-β1 and another known tumor suppressor gene (TSG) Merlin. Down-regulation of Integrin-β1 or Merlin was significantly correlated with the poor survival rate of NPC patients. Further mechanistic studies showed that CHL1 could directly interact with integrin-β1 and link to Merlin, leading to the inactivation of integrin β1-AKT pathway. In conclusion, CHL1 is a vital tumor suppressor in the carcinogenesis of NPC.
Persistent Identifierhttp://hdl.handle.net/10722/278066
ISSN
2017 Impact Factor: 4.057
2015 SCImago Journal Rankings: 1.927
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorChen, J-
dc.contributor.authorJIANG, C-
dc.contributor.authorFu, L-
dc.contributor.authorZhu, C-L-
dc.contributor.authorXiang, Y-Q-
dc.contributor.authorJiang, L-X-
dc.contributor.authorChen, Q-
dc.contributor.authorLin, WM-
dc.contributor.authorCHEN, J-N-
dc.contributor.authorZhang, L-Y-
dc.contributor.authorLiu, M-
dc.contributor.authorChen, C-
dc.contributor.authorTang, H-
dc.contributor.authorWang, B-
dc.contributor.authorTsao, SW-
dc.contributor.authorKwong, DLW-
dc.contributor.authorGuan, X-
dc.date.accessioned2019-10-04T08:06:51Z-
dc.date.available2019-10-04T08:06:51Z-
dc.date.issued2019-
dc.identifier.citationInternational Journal of Biological Sciences, 2019, v. 15 n. 9, p. 1802-1815-
dc.identifier.issn1449-2288-
dc.identifier.urihttp://hdl.handle.net/10722/278066-
dc.description.abstractDeletion of Chromosome 3p is one of the most frequently detected genetic alterations in nasopharyngeal carcinoma (NPC). We reported the role of a novel 3p26.3 tumor suppressor gene (TSG) CHL1 in NPC. Down-regulation of CHL1 was detected in 4/6 of NPC cell lines and 71/95 (74.7%) in clinical tissues. Ectopic expressions of CHL1 in NPC cells significantly inhibit colony formation and cell motility in functional study. By up-regulating epithelial markers and down-regulating mesenchymal markers CHL1 could induce mesenchymal-epithelial transition (MET), a key step in preventing tumor invasion and metastasis. CHL1 could also cause the inactivation of RhoA/Rac1/Cdc42 signaling pathway and inhibit the formation of stress fiber, lamellipodia, and filopodia. CHL1 could co-localize with adhesion molecule Integrin-β1, the expression of CHL1 was positively correlated with Integrin-β1 and another known tumor suppressor gene (TSG) Merlin. Down-regulation of Integrin-β1 or Merlin was significantly correlated with the poor survival rate of NPC patients. Further mechanistic studies showed that CHL1 could directly interact with integrin-β1 and link to Merlin, leading to the inactivation of integrin β1-AKT pathway. In conclusion, CHL1 is a vital tumor suppressor in the carcinogenesis of NPC.-
dc.languageeng-
dc.publisherIvyspring International Publisher. The Journal's web site is located at http://www.biolsci.org/index.htm-
dc.relation.ispartofInternational Journal of Biological Sciences-
dc.rightsInternational Journal of Biological Sciences. Copyright © Ivyspring International Publisher.-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectnasopharyngeal carcinoma-
dc.subjecttumor suppressor gene-
dc.subjecttumor invasion-
dc.subjecttumor metastasis-
dc.titleCHL1 suppresses tumor growth and metastasis in nasopharyngeal carcinoma by repressing PI3K/AKT signaling pathway via interaction with Integrin β1 and Merlin-
dc.typeArticle-
dc.identifier.emailTsao, SW: gswtsao@hku.hk-
dc.identifier.emailKwong, DLW: dlwkwong@hku.hk-
dc.identifier.emailGuan, X: xyguan@hku.hk-
dc.identifier.authorityTsao, SW=rp00399-
dc.identifier.authorityKwong, DLW=rp00414-
dc.identifier.authorityGuan, X=rp00454-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.7150/ijbs.34785-
dc.identifier.pmid31523184-
dc.identifier.pmcidPMC6743306-
dc.identifier.scopuseid_2-s2.0-85070992520-
dc.identifier.hkuros306348-
dc.identifier.volume15-
dc.identifier.issue9-
dc.identifier.spage1802-
dc.identifier.epage1815-
dc.publisher.placeAustralia-

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