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Conference Paper: Functional role of caveolin-1-mediated S100P signaling in liver cancer metastasis under hypoxia

TitleFunctional role of caveolin-1-mediated S100P signaling in liver cancer metastasis under hypoxia
Authors
Issue Date2016
PublisherSpringer New York LLC. The Journal's web site is located at http://www.springer.com/west/home/medicine?SGWID=4-10054-70-173733513-0
Citation
The 25th Conference of the Asian Pacific Association for the Study of the Liver (APASL 2016), Tokyo Japan, 20-24 February 2016. In Hepatology International, 2016, v. 10 n. 1 suppl., p. S292, abstract no. P-0558 How to Cite?
AbstractHypoxia is a common feature of hepatocellular carcinoma (HCC) and facilitates tumor metastasis. High level of Caveolin-1 (Cav1) was exclusively expressed in primary HCC and metastatic tissues and its level was further enhanced under hypoxic stress. Suppression of Cav1 reduced HCC growth and metastasis. However, the potential role of Cav1 in human cancers under hypoxic stress has never been reported. A cDNA array profiling identified S100P calcium binding protein as a downstream target of Cav1. S100P is highly expressed in several malignancies and promote metastasis. In the present study, we showed that S100P expression was well correlated with Cav1 expression in a panel of HCC cell lines. In addition, S100P expression at protein and mRNA levels was largely suppressed in sh-Cav1 knockdown cells. Suppression of S100P expression largely inhibited tumorigenesis in subcutaneous injection and orthotopic liver implantation models. Furthermore, hypoxia significantly enhanced the migration and invasion of control and such enhancement was not prominent when Cav1 or S100P was suppressed. Taking together, Cav1 functions as the upstream component of S100P and plays a critical role in modulation of cell motility during hypoxia. Thereafter, our data showed Cav1 was able to activate NF-jB reporter and transient expression of Cav1 upregulated S100P in cells. Addition of NF-jB inhibitor, IMD-0354 abolished the upregulation of S100P by Cav1 suggests that Cav1 upregulates S100P via the activation of NFjB pathway. In conclusion, Cav1 may upregulate S100P through the activation of NF-jB cascade to confer the enhanced aggressiveness of HCC cells under hypoxic condition.
DescriptionPoster Presentation: P-0558
This journal suppl. entitled: Abstracts of the 25th Annual Conference of APASL, February 20–24, 2016, Tokyo, Japan
Persistent Identifierhttp://hdl.handle.net/10722/229933
ISSN
2015 Impact Factor: 1.125
2015 SCImago Journal Rankings: 0.669

 

DC FieldValueLanguage
dc.contributor.authorMao, X-
dc.contributor.authorWong, SYS-
dc.contributor.authorKo, FCF-
dc.contributor.authorYam, JWP-
dc.date.accessioned2016-08-23T14:14:10Z-
dc.date.available2016-08-23T14:14:10Z-
dc.date.issued2016-
dc.identifier.citationThe 25th Conference of the Asian Pacific Association for the Study of the Liver (APASL 2016), Tokyo Japan, 20-24 February 2016. In Hepatology International, 2016, v. 10 n. 1 suppl., p. S292, abstract no. P-0558-
dc.identifier.issn1936-0533-
dc.identifier.urihttp://hdl.handle.net/10722/229933-
dc.descriptionPoster Presentation: P-0558-
dc.descriptionThis journal suppl. entitled: Abstracts of the 25th Annual Conference of APASL, February 20–24, 2016, Tokyo, Japan-
dc.description.abstractHypoxia is a common feature of hepatocellular carcinoma (HCC) and facilitates tumor metastasis. High level of Caveolin-1 (Cav1) was exclusively expressed in primary HCC and metastatic tissues and its level was further enhanced under hypoxic stress. Suppression of Cav1 reduced HCC growth and metastasis. However, the potential role of Cav1 in human cancers under hypoxic stress has never been reported. A cDNA array profiling identified S100P calcium binding protein as a downstream target of Cav1. S100P is highly expressed in several malignancies and promote metastasis. In the present study, we showed that S100P expression was well correlated with Cav1 expression in a panel of HCC cell lines. In addition, S100P expression at protein and mRNA levels was largely suppressed in sh-Cav1 knockdown cells. Suppression of S100P expression largely inhibited tumorigenesis in subcutaneous injection and orthotopic liver implantation models. Furthermore, hypoxia significantly enhanced the migration and invasion of control and such enhancement was not prominent when Cav1 or S100P was suppressed. Taking together, Cav1 functions as the upstream component of S100P and plays a critical role in modulation of cell motility during hypoxia. Thereafter, our data showed Cav1 was able to activate NF-jB reporter and transient expression of Cav1 upregulated S100P in cells. Addition of NF-jB inhibitor, IMD-0354 abolished the upregulation of S100P by Cav1 suggests that Cav1 upregulates S100P via the activation of NFjB pathway. In conclusion, Cav1 may upregulate S100P through the activation of NF-jB cascade to confer the enhanced aggressiveness of HCC cells under hypoxic condition.-
dc.languageeng-
dc.publisherSpringer New York LLC. The Journal's web site is located at http://www.springer.com/west/home/medicine?SGWID=4-10054-70-173733513-0-
dc.relation.ispartofHepatology International-
dc.rightsThe final publication is available at Springer via http://dx.doi.org/10.1007/s12072-016-9707-8-
dc.titleFunctional role of caveolin-1-mediated S100P signaling in liver cancer metastasis under hypoxia-
dc.typeConference_Paper-
dc.identifier.emailMao, X: susanmao@hku.hk-
dc.identifier.emailKo, FCF: bokcf@hku.hk-
dc.identifier.emailYam, JWP: judyyam@pathology.hku.hk-
dc.identifier.authorityYam, JWP=rp00468-
dc.identifier.doi10.1007/s12072-016-9707-8-
dc.identifier.hkuros261342-
dc.identifier.volume10-
dc.identifier.issue1 suppl.-
dc.identifier.spageS292, abstract no. P-0558-
dc.identifier.epageS292, abstract no. P-0558-
dc.publisher.placeUnited States-

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