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Article: Over-expression of miR-106b promotes cell migration and metastasis in hepatocellular carcinoma by activating epithelial-mesenchymal transition process

TitleOver-expression of miR-106b promotes cell migration and metastasis in hepatocellular carcinoma by activating epithelial-mesenchymal transition process
Authors
Issue Date2013
Citation
PLoS One, 2013, v. 8 n. 3, p. e57882 How to Cite?
AbstractHepatocellular carcinoma (HCC) is one the the most fatal cancers worldwide. The poor prognosis of HCC is mainly due to the developement of distance metastasis. To investigate the mechanism of metastasis in HCC, an orthotopic HCC metastasis animal model was established. Two sets of primary liver tumor cell lines and corresponding lung metastasis cell lines were generated. In vitro functional analysis demonstrated that the metastatic cell line had higher invasion and migration ability when compared with the primary liver tumor cell line. These cell lines were subjected to microRNA (miRNAs) microarray analysis to identify differentially expressed miRNAs which were associated with the developement of metastasis in vivo. Fifteen human miRNAs, including miR-106b, were differentially expressed in 2 metastatic cell lines compared with the primary tumor cell lines. The clinical significance of miR-106b in 99 HCC clinical samples was studied. The results demonstrated that miR-106b was over-expressed in HCC tumor tissue compared with adjacent non-tumor tissue (p = 0.0005), and overexpression of miR-106b was signficantly correlated with higher tumor grade (p = 0.018). Further functional studies demonstrated that miR-106b could promote cell migration and stress fiber formation by over-expressing RhoGTPases, RhoA and RhoC. In vivo functional studies also showed that over-expression of miR-106b promoted HCC metastasis. These effects were related to the activation of the epithelial-mesenchymal transition (EMT) process. Our results suggested that miR-106b expression contributed to HCC metastasis by activating the EMT process promoting cell migration in vitro and metastasis in vivo. © 2013 Yau et al.
Persistent Identifierhttp://hdl.handle.net/10722/182031
ISSN
2015 Impact Factor: 3.057
2015 SCImago Journal Rankings: 1.395

 

DC FieldValueLanguage
dc.contributor.authorYau, WLen_US
dc.contributor.authorLam, SCen_US
dc.contributor.authorNg, Len_US
dc.contributor.authorChow, KMen_US
dc.contributor.authorChan, TCen_US
dc.contributor.authorChan, JYKen_US
dc.contributor.authorWo, YHen_US
dc.contributor.authorNg, KTPen_US
dc.contributor.authorMan, Ken_US
dc.contributor.authorPoon, RTPen_US
dc.contributor.authorPang, RWCen_US
dc.date.accessioned2013-04-17T07:19:16Z-
dc.date.available2013-04-17T07:19:16Z-
dc.date.issued2013en_US
dc.identifier.citationPLoS One, 2013, v. 8 n. 3, p. e57882en_US
dc.identifier.issn1932-6203-
dc.identifier.urihttp://hdl.handle.net/10722/182031-
dc.description.abstractHepatocellular carcinoma (HCC) is one the the most fatal cancers worldwide. The poor prognosis of HCC is mainly due to the developement of distance metastasis. To investigate the mechanism of metastasis in HCC, an orthotopic HCC metastasis animal model was established. Two sets of primary liver tumor cell lines and corresponding lung metastasis cell lines were generated. In vitro functional analysis demonstrated that the metastatic cell line had higher invasion and migration ability when compared with the primary liver tumor cell line. These cell lines were subjected to microRNA (miRNAs) microarray analysis to identify differentially expressed miRNAs which were associated with the developement of metastasis in vivo. Fifteen human miRNAs, including miR-106b, were differentially expressed in 2 metastatic cell lines compared with the primary tumor cell lines. The clinical significance of miR-106b in 99 HCC clinical samples was studied. The results demonstrated that miR-106b was over-expressed in HCC tumor tissue compared with adjacent non-tumor tissue (p = 0.0005), and overexpression of miR-106b was signficantly correlated with higher tumor grade (p = 0.018). Further functional studies demonstrated that miR-106b could promote cell migration and stress fiber formation by over-expressing RhoGTPases, RhoA and RhoC. In vivo functional studies also showed that over-expression of miR-106b promoted HCC metastasis. These effects were related to the activation of the epithelial-mesenchymal transition (EMT) process. Our results suggested that miR-106b expression contributed to HCC metastasis by activating the EMT process promoting cell migration in vitro and metastasis in vivo. © 2013 Yau et al.-
dc.languageengen_US
dc.relation.ispartofPLoS Oneen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleOver-expression of miR-106b promotes cell migration and metastasis in hepatocellular carcinoma by activating epithelial-mesenchymal transition processen_US
dc.typeArticleen_US
dc.identifier.emailYau, WL: swlyau@hku.hken_US
dc.identifier.emailLam, SC: colin88@hku.hken_US
dc.identifier.emailNg, L: luing@hku.hken_US
dc.identifier.emailChow, KM: chowakm@hku.hken_US
dc.identifier.emailChan, JYK: jykchan6@hkucc.hku.hken_US
dc.identifier.emailWo, YH: woyh@hku.hken_US
dc.identifier.emailNg, KTP: ledodes@hku.hken_US
dc.identifier.emailMan, K: kwanman@hku.hken_US
dc.identifier.emailPoon, RTP: poontp@hku.hken_US
dc.identifier.emailPang, RWC: robertap@hku.hken_US
dc.identifier.authorityNg, KTP=rp01720en_US
dc.identifier.authorityMan, K=rp00417en_US
dc.identifier.authorityPoon, RTP=rp00446en_US
dc.identifier.authorityPang, RWC=rp00274en_US
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pone.0057882-
dc.identifier.pmid23483935-
dc.identifier.scopuseid_2-s2.0-84874595113-
dc.identifier.hkuros213828en_US
dc.identifier.volume8en_US
dc.identifier.issue3en_US
dc.identifier.spagee57882en_US
dc.identifier.epagee57882en_US

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