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Conference Paper: Functional characterization of novel tumour suppressor galectin-2 in hepatocellular carcinoma

TitleFunctional characterization of novel tumour suppressor galectin-2 in hepatocellular carcinoma
Authors
Issue Date2016
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/ejca
Citation
The 24th Biennial Congress of the European Association for Cancer Research (EACR-24), Manchester, UK., 9-12 July 2016. In European Journal of Cancer, 2016, v. 61 suppl. 1, p. S62, abstract no. 318 How to Cite?
AbstractBACKGROUND: Hepatocellular carcinoma (HCC) is the second most common cause of cancer mortality in the world. The development of HCC, hepatocarcinogenesis, is a multistep progression. However, the prognosis of HCC is predominantly poor and has a low survival rate because of its late presentation, high incidence of recurrence and metastasis resulting in limited therapeutic options. From our previous studies, tumour suppressor Deleted in liver cancer 1 (DLC1) is a crucial RhoGTP activating protein (RhoGAP) for HCC development. In our screening study, we identified galectin-2 as a downstream target protein of the DLC1 pathway. Hence, the characteristic of galectin-2 expression has triggered us to study its clinical significance and functional role in HCC in further details. MATERIAL AND METHODS: This project is divided into two main sections: 1) analysis of clinical correlation of galectin-2 expression in HCC cell lines and tissues and 2) functional characterization of galectin-2 in HCC tumourigenesis and metastasis. RESULTS: For clinical analysis of galectin-2 expression in HCC, around fifty HCC patient samples were examined. The results showed that the expression of galectin-2 was significantly underexpressed in HCC tumorous tissues when compared to the corresponding non-tumorous liver tissues. Galectin-2 expression was also directly correlated to DLC1 expression. Additionally, underexpression of galectin-2 was significantly associated with poor overall survival. In HCC cell line panel, galectin-2 was dramatically expressed in an immortalized liver cell line MIHA; in contrast, it was downregulated in both the non-metastatic and metastatic HCC cell lines. To address the functional roles of galectin-2 in HCC, the abilities of galectin-2 to regulate cell proliferation, cell migration and cell invasion were analyzed in the tetracycline inducible (Tet-on) cell line model by expressing galectin-2 in metastatic MHCC-97L cells. The results illustrated that galectin-2 significantly inhibited cell proliferation, migration and invasion in HCC metastatic cells. Furthermore, the ability of galectin-2 in suppressing tumor development was revealed in the in vivo study via subcutaneous injection in nude mice performed with galectin-2 expressing metastatic MHCC-97L cells. CONCLUSIONS: In this study, the clinical relevance of galectin-2 revealed its underexpression in HCC and its association with poorer prognosis. Functionally, galectin-2 was demonstrated to inhibit growth, motility and tumorigenesis of HCC. Further investigation for the detail underlying the interplay between DLC1 and galectin-2 will also be discussed and will be crucial in the understanding of underlying basis of HCC tumorigenesis.
DescriptionConference Theme: From basic research to precision medicine
Poster Session: Cell and Tumour Biology 1: no. 318
This journal suppl. entitled: 24th Biennial Congress of the European Association for Cancer Research, 9–12 July 2016, Manchester, UK
Persistent Identifierhttp://hdl.handle.net/10722/229932
ISSN
2015 Impact Factor: 6.163
2015 SCImago Journal Rankings: 3.152

 

DC FieldValueLanguage
dc.contributor.authorKo, FCF-
dc.contributor.authorLee, KW-
dc.contributor.authorTai, WCS-
dc.contributor.authorLeung, Z-
dc.contributor.authorYam, JWP-
dc.date.accessioned2016-08-23T14:14:09Z-
dc.date.available2016-08-23T14:14:09Z-
dc.date.issued2016-
dc.identifier.citationThe 24th Biennial Congress of the European Association for Cancer Research (EACR-24), Manchester, UK., 9-12 July 2016. In European Journal of Cancer, 2016, v. 61 suppl. 1, p. S62, abstract no. 318-
dc.identifier.issn0959-8049-
dc.identifier.urihttp://hdl.handle.net/10722/229932-
dc.descriptionConference Theme: From basic research to precision medicine-
dc.descriptionPoster Session: Cell and Tumour Biology 1: no. 318-
dc.descriptionThis journal suppl. entitled: 24th Biennial Congress of the European Association for Cancer Research, 9–12 July 2016, Manchester, UK-
dc.description.abstractBACKGROUND: Hepatocellular carcinoma (HCC) is the second most common cause of cancer mortality in the world. The development of HCC, hepatocarcinogenesis, is a multistep progression. However, the prognosis of HCC is predominantly poor and has a low survival rate because of its late presentation, high incidence of recurrence and metastasis resulting in limited therapeutic options. From our previous studies, tumour suppressor Deleted in liver cancer 1 (DLC1) is a crucial RhoGTP activating protein (RhoGAP) for HCC development. In our screening study, we identified galectin-2 as a downstream target protein of the DLC1 pathway. Hence, the characteristic of galectin-2 expression has triggered us to study its clinical significance and functional role in HCC in further details. MATERIAL AND METHODS: This project is divided into two main sections: 1) analysis of clinical correlation of galectin-2 expression in HCC cell lines and tissues and 2) functional characterization of galectin-2 in HCC tumourigenesis and metastasis. RESULTS: For clinical analysis of galectin-2 expression in HCC, around fifty HCC patient samples were examined. The results showed that the expression of galectin-2 was significantly underexpressed in HCC tumorous tissues when compared to the corresponding non-tumorous liver tissues. Galectin-2 expression was also directly correlated to DLC1 expression. Additionally, underexpression of galectin-2 was significantly associated with poor overall survival. In HCC cell line panel, galectin-2 was dramatically expressed in an immortalized liver cell line MIHA; in contrast, it was downregulated in both the non-metastatic and metastatic HCC cell lines. To address the functional roles of galectin-2 in HCC, the abilities of galectin-2 to regulate cell proliferation, cell migration and cell invasion were analyzed in the tetracycline inducible (Tet-on) cell line model by expressing galectin-2 in metastatic MHCC-97L cells. The results illustrated that galectin-2 significantly inhibited cell proliferation, migration and invasion in HCC metastatic cells. Furthermore, the ability of galectin-2 in suppressing tumor development was revealed in the in vivo study via subcutaneous injection in nude mice performed with galectin-2 expressing metastatic MHCC-97L cells. CONCLUSIONS: In this study, the clinical relevance of galectin-2 revealed its underexpression in HCC and its association with poorer prognosis. Functionally, galectin-2 was demonstrated to inhibit growth, motility and tumorigenesis of HCC. Further investigation for the detail underlying the interplay between DLC1 and galectin-2 will also be discussed and will be crucial in the understanding of underlying basis of HCC tumorigenesis.-
dc.languageeng-
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/ejca-
dc.relation.ispartofEuropean Journal of Cancer-
dc.rightsPosting accepted manuscript (postprint): © 2016. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/-
dc.titleFunctional characterization of novel tumour suppressor galectin-2 in hepatocellular carcinoma-
dc.typeConference_Paper-
dc.identifier.emailKo, FCF: bokcf@hku.hk-
dc.identifier.emailLee, KW: tkwlee@hkucc.hku.hk-
dc.identifier.emailYam, JWP: judyyam@pathology.hku.hk-
dc.identifier.authorityLee, KW=rp00447-
dc.identifier.authorityYam, JWP=rp00468-
dc.identifier.doi10.1016/S0959-8049(16)61214-5-
dc.identifier.hkuros261340-
dc.identifier.volume61-
dc.identifier.issuesuppl. 1-
dc.identifier.spageS62, abstract no. 318-
dc.identifier.epageS62, abstract no. 318-
dc.publisher.placeUnited Kingdom-

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