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Article: HN1L-mediated transcriptional axis AP-2γ/METTL13/TCF3-ZEB1 drives tumor growth and metastasis in hepatocellular carcinoma

TitleHN1L-mediated transcriptional axis AP-2γ/METTL13/TCF3-ZEB1 drives tumor growth and metastasis in hepatocellular carcinoma
Authors
KeywordsMetastasis
Oncogenes
Tumour biomarkers
Issue Date2019
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/cdd
Citation
Cell Death and Differentiation, 2019, v. 26 n. 11, p. 2268-2283 How to Cite?
AbstractHepatocellular carcinoma (HCC) is one of the most aggressive malignancies and lacks targeted therapies. Here, we reported a novel potential therapeutic target hematological and neurological expressed 1 like (HN1L) in HCC. First, HCC tissue microarray analysis showed that HN1L was frequently up-regulated in cancer tissues than that in normal liver tissues, which significantly associated with tumor size, local invasion, distant metastases, and poor prognosis for HCC patients. Functional studies demonstrated that ectopic expression of HN1L could increase cell growth, foci formation in monolayer culture, colony formation in soft agar and tumorigenesis in nude mice. In addition, HN1L could also promote HCC metastasis by inducing epithelial-mesenchymal transition. Inversely, silencing HN1L expression with shRNA could effectively attenuate its oncogenic function. We further showed that HN1L transcriptionally up-regulated methyltransferase like 13 (METTL13) gene in an AP-2γ dependent manner, which promoted cell proliferation and metastasis by up-regulating TCF3 and ZEB1. Importantly, administration of lentivirus-mediated shRNA interfering HN1L expression could inhibit tumorigenesis and metastasis in mice. Collectively, HN1L-mediated transcriptional axis AP-2γ/METTL13/TCF3-ZEB1 promotes HCC growth and metastasis representing a promising therapeutic target in HCC treatment.
Persistent Identifierhttp://hdl.handle.net/10722/284548
ISSN
2019 Impact Factor: 10.717
2015 SCImago Journal Rankings: 4.219
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorLi, L-
dc.contributor.authorZheng, YL-
dc.contributor.authorJIANG, C-
dc.contributor.authorFANG, S-
dc.contributor.authorZeng, TT-
dc.contributor.authorZhu, YH-
dc.contributor.authorLi, Y-
dc.contributor.authorXie, D-
dc.contributor.authorGuan, XY-
dc.date.accessioned2020-08-07T08:59:13Z-
dc.date.available2020-08-07T08:59:13Z-
dc.date.issued2019-
dc.identifier.citationCell Death and Differentiation, 2019, v. 26 n. 11, p. 2268-2283-
dc.identifier.issn1350-9047-
dc.identifier.urihttp://hdl.handle.net/10722/284548-
dc.description.abstractHepatocellular carcinoma (HCC) is one of the most aggressive malignancies and lacks targeted therapies. Here, we reported a novel potential therapeutic target hematological and neurological expressed 1 like (HN1L) in HCC. First, HCC tissue microarray analysis showed that HN1L was frequently up-regulated in cancer tissues than that in normal liver tissues, which significantly associated with tumor size, local invasion, distant metastases, and poor prognosis for HCC patients. Functional studies demonstrated that ectopic expression of HN1L could increase cell growth, foci formation in monolayer culture, colony formation in soft agar and tumorigenesis in nude mice. In addition, HN1L could also promote HCC metastasis by inducing epithelial-mesenchymal transition. Inversely, silencing HN1L expression with shRNA could effectively attenuate its oncogenic function. We further showed that HN1L transcriptionally up-regulated methyltransferase like 13 (METTL13) gene in an AP-2γ dependent manner, which promoted cell proliferation and metastasis by up-regulating TCF3 and ZEB1. Importantly, administration of lentivirus-mediated shRNA interfering HN1L expression could inhibit tumorigenesis and metastasis in mice. Collectively, HN1L-mediated transcriptional axis AP-2γ/METTL13/TCF3-ZEB1 promotes HCC growth and metastasis representing a promising therapeutic target in HCC treatment.-
dc.languageeng-
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/cdd-
dc.relation.ispartofCell Death and Differentiation-
dc.rightsThis is a post-peer-review, pre-copyedit version of an article published in [insert journal title]. The final authenticated version is available online at: https://doi.org/[insert DOI]-
dc.subjectMetastasis-
dc.subjectOncogenes-
dc.subjectTumour biomarkers-
dc.titleHN1L-mediated transcriptional axis AP-2γ/METTL13/TCF3-ZEB1 drives tumor growth and metastasis in hepatocellular carcinoma-
dc.typeArticle-
dc.identifier.emailLi, L: lilei728@hku.hk-
dc.identifier.emailGuan, XY: xyguan@hku.hk-
dc.identifier.authorityGuan, XY=rp00454-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1038/s41418-019-0301-1-
dc.identifier.pmid30778199-
dc.identifier.pmcidPMC6889153-
dc.identifier.scopuseid_2-s2.0-85061739422-
dc.identifier.hkuros312296-
dc.identifier.volume26-
dc.identifier.issue11-
dc.identifier.spage2268-
dc.identifier.epage2283-
dc.publisher.placeUnited Kingdom-

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