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Article: Cylindromatosis Lysine 63 Deubiquitinase (CYLD) Regulates NF-kB Signaling Pathway and Modulates Fibroblast and Endothelial Cells Recruitment in Nasopharyngeal Carcinoma

TitleCylindromatosis Lysine 63 Deubiquitinase (CYLD) Regulates NF-kB Signaling Pathway and Modulates Fibroblast and Endothelial Cells Recruitment in Nasopharyngeal Carcinoma
Authors
KeywordsNF-kB
cylindromatosis lysine 63 deubiquitinase (CYLD)
nasopharyngeal carcinoma (NPC)
tumor microenvironment
Issue Date2020
PublisherMDPI AG. The Journal's web site is located at http://www.mdpi.com/journal/cancers/
Citation
Cancers, 2020, v. 12 n. 7, article no. 1924 How to Cite?
AbstractNasopharyngeal carcinoma (NPC) is a malignant epithelial carcinoma of the nasopharynx. Cylindromatosis lysine 63 deubiquitinase (CYLD), a NF-kB inhibitor, was reported as one of the top mutated candidate genes in NPC. NF-kB is an inducible transcription factor, contributing to cancer via regulating inflammation, angiogenesis, cell proliferation, and metastasis. In this study, the impact of CYLD on regulating the NF-kB signaling pathway and its contribution to NPC development was studied using in vitro and in vivo functional assays, together with single cell RNA sequencing to understand the NPC tumor microenvironment. CYLD was downregulated in NPC clinical specimens and multiple cell lines. Functional assays revealed CYLD inhibits NPC cell proliferation and migration in vitro and suppresses NPC tumorigenicity and metastasis in vivo by negatively regulating the NF-kB signaling pathway. Additionally, CYLD was able to inhibit fibroblast and endothelial stromal cell infiltration into the NPC tumor microenvironment. These findings suggest that CYLD inhibits NPC development and provides strong evidence supporting a role for CYLD inhibiting fibroblast and endothelial stromal cell infiltration into NPC via suppressing the NF-kB pathway.
Persistent Identifierhttp://hdl.handle.net/10722/286196
ISSN
2021 Impact Factor: 6.575
2020 SCImago Journal Rankings: 1.818
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorDeng, M-
dc.contributor.authorDai, W-
dc.contributor.authorYu, VZ-
dc.contributor.authorTao, L-
dc.contributor.authorLung, ML-
dc.date.accessioned2020-08-31T07:00:30Z-
dc.date.available2020-08-31T07:00:30Z-
dc.date.issued2020-
dc.identifier.citationCancers, 2020, v. 12 n. 7, article no. 1924-
dc.identifier.issn2072-6694-
dc.identifier.urihttp://hdl.handle.net/10722/286196-
dc.description.abstractNasopharyngeal carcinoma (NPC) is a malignant epithelial carcinoma of the nasopharynx. Cylindromatosis lysine 63 deubiquitinase (CYLD), a NF-kB inhibitor, was reported as one of the top mutated candidate genes in NPC. NF-kB is an inducible transcription factor, contributing to cancer via regulating inflammation, angiogenesis, cell proliferation, and metastasis. In this study, the impact of CYLD on regulating the NF-kB signaling pathway and its contribution to NPC development was studied using in vitro and in vivo functional assays, together with single cell RNA sequencing to understand the NPC tumor microenvironment. CYLD was downregulated in NPC clinical specimens and multiple cell lines. Functional assays revealed CYLD inhibits NPC cell proliferation and migration in vitro and suppresses NPC tumorigenicity and metastasis in vivo by negatively regulating the NF-kB signaling pathway. Additionally, CYLD was able to inhibit fibroblast and endothelial stromal cell infiltration into the NPC tumor microenvironment. These findings suggest that CYLD inhibits NPC development and provides strong evidence supporting a role for CYLD inhibiting fibroblast and endothelial stromal cell infiltration into NPC via suppressing the NF-kB pathway.-
dc.languageeng-
dc.publisherMDPI AG. The Journal's web site is located at http://www.mdpi.com/journal/cancers/-
dc.relation.ispartofCancers-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectNF-kB-
dc.subjectcylindromatosis lysine 63 deubiquitinase (CYLD)-
dc.subjectnasopharyngeal carcinoma (NPC)-
dc.subjecttumor microenvironment-
dc.titleCylindromatosis Lysine 63 Deubiquitinase (CYLD) Regulates NF-kB Signaling Pathway and Modulates Fibroblast and Endothelial Cells Recruitment in Nasopharyngeal Carcinoma-
dc.typeArticle-
dc.identifier.emailDeng, M: mddeng@hku.hk-
dc.identifier.emailDai, W: weidai2@hku.hk-
dc.identifier.emailYu, VZ: zvyu@hku.hk-
dc.identifier.emailTao, L: taolihua@hku.hk-
dc.identifier.emailLung, ML: mlilung@hku.hk-
dc.identifier.authorityDai, W=rp02146-
dc.identifier.authorityLung, ML=rp00300-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.3390/cancers12071924-
dc.identifier.pmid32708712-
dc.identifier.pmcidPMC7409113-
dc.identifier.scopuseid_2-s2.0-85088486901-
dc.identifier.hkuros313276-
dc.identifier.volume12-
dc.identifier.issue7-
dc.identifier.spagearticle no. 1924-
dc.identifier.epagearticle no. 1924-
dc.identifier.isiWOS:000554770000001-
dc.publisher.placeSwitzerland-
dc.identifier.issnl2072-6694-

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