File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Conference Paper: TTC36, a novel chaperone of heat shock protein 70, functions as a tumor suppressor in hepatocellular carcinoma

TitleTTC36, a novel chaperone of heat shock protein 70, functions as a tumor suppressor in hepatocellular carcinoma
Authors
Issue Date2014
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
Proceedings of 105th American Association for Cancer Research (AACR) Annual Meeting 2014, San Diego, CA, USA, 5-9 April 2014. In Cancer Research, 2014, v. 74 n. 19, Suppl., p. Abstract no. 1559 How to Cite?
AbstractHepatocellular carcinoma (HCC) is one of the most devastating human diseases characterized by high incidences and mortality rates. However, there is still limited knowledge of molecular mechanisms leading to the development of HCC. By using transcriptome sequencing profiling of non-tumor and HCC samples, a subset of differentially expressed genes have been identified. One of those genes, the TTC36 gene is down-regulated in HCC tissues compared with non-tumor tissues. Reduced expression of TTC36 is correlated with advanced tumor stages and decreased overall survival. Ectopic expression of TTC36 in HCC cells show decreased tumorigenic ability in vitro and vivo function assays. Silencing TTC36 expression with short hairpin RNA had the opposite effects. We had found that TTC36 promoted apoptosis of HCC cells by interacting with heat shock protein 70 and induced the activation of caspases-9, caspase-3 and PARP. Further characterization of TTC36 may provide a novel prognostic biomarker for HCC and shed light on better management of HCC treatment. Note: This abstract was not presented at the meeting.
Persistent Identifierhttp://hdl.handle.net/10722/246157
ISSN
2021 Impact Factor: 13.312
2020 SCImago Journal Rankings: 4.103
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorJiang, L-
dc.contributor.authorLiu, M-
dc.contributor.authorLi, Y-
dc.contributor.authorGuan, X-
dc.date.accessioned2017-09-18T02:23:26Z-
dc.date.available2017-09-18T02:23:26Z-
dc.date.issued2014-
dc.identifier.citationProceedings of 105th American Association for Cancer Research (AACR) Annual Meeting 2014, San Diego, CA, USA, 5-9 April 2014. In Cancer Research, 2014, v. 74 n. 19, Suppl., p. Abstract no. 1559-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/246157-
dc.description.abstractHepatocellular carcinoma (HCC) is one of the most devastating human diseases characterized by high incidences and mortality rates. However, there is still limited knowledge of molecular mechanisms leading to the development of HCC. By using transcriptome sequencing profiling of non-tumor and HCC samples, a subset of differentially expressed genes have been identified. One of those genes, the TTC36 gene is down-regulated in HCC tissues compared with non-tumor tissues. Reduced expression of TTC36 is correlated with advanced tumor stages and decreased overall survival. Ectopic expression of TTC36 in HCC cells show decreased tumorigenic ability in vitro and vivo function assays. Silencing TTC36 expression with short hairpin RNA had the opposite effects. We had found that TTC36 promoted apoptosis of HCC cells by interacting with heat shock protein 70 and induced the activation of caspases-9, caspase-3 and PARP. Further characterization of TTC36 may provide a novel prognostic biomarker for HCC and shed light on better management of HCC treatment. Note: This abstract was not presented at the meeting.-
dc.languageeng-
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/-
dc.relation.ispartofCancer Research-
dc.titleTTC36, a novel chaperone of heat shock protein 70, functions as a tumor suppressor in hepatocellular carcinoma-
dc.typeConference_Paper-
dc.identifier.emailGuan, X: xyguan@hkucc.hku.hk-
dc.identifier.authorityGuan, X=rp00454-
dc.identifier.doi10.1158/1538-7445.AM2014-1559-
dc.identifier.hkuros276957-
dc.identifier.volume74-
dc.identifier.issue19, Suppl.-
dc.identifier.spageAbstract no. 1559-
dc.identifier.epageAbstract no. 1559-
dc.identifier.isiWOS:000349906901285-
dc.publisher.placeUnited States-
dc.identifier.issnl0008-5472-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats