Histone deacetylase inhibitors enhance the apoptotic activity of insulin-like growth factor binding protein-3 by blocking PKC-induced IGFBP-3 degradation
DC Field | Value | Language |
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dc.contributor.author | Oh, Seung Hyun | - |
dc.contributor.author | Whang, Young Mi | - |
dc.contributor.author | Min, Hye-Young | - |
dc.contributor.author | Han, Seung Ho | - |
dc.contributor.author | Kang, Ju-Hee | - |
dc.contributor.author | Song, Ki-Hoon | - |
dc.contributor.author | Glisson, Bonnie S. | - |
dc.contributor.author | Kim, Yeul Hong | - |
dc.contributor.author | Lee, Ho-Young | - |
dc.date.available | 2020-02-29T04:45:45Z | - |
dc.date.created | 2020-02-06 | - |
dc.date.issued | 2012-11-15 | - |
dc.identifier.issn | 0020-7136 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/16011 | - |
dc.description.abstract | Overexpression of insulin-like growth factor binding protein (IGFBP)-3 induces apoptosis of cancer cells. However, preexisting resistance to IGFBP-3 could limit its antitumor activities. This study characterizes the efficacy and mechanism of the combination of recombinant IGFBP-3 (rIGFBP-3) and HDAC inhibitors to overcome IGFBP-3 resistance in a subset of non-small cell lung cancer (NSCLC) and head and neck squamous cell carcinoma (HNSCC) cells. The effects of the combination of rIGFBP-3 and a number of HDAC inhibitors on cell proliferation and apoptosis were assessed in vitro and in vivo by using the MTT assay, a flow cytometry-based TUNEL assay, Western blot analyses and the NSCLC xenograft tumor model. Combined treatment with HDAC inhibitors and rIGFBP-3 had synergistic antiproliferative effects accompanied by increased apoptosis rates in a subset of NSCLC and HNSCC cell lines in vitro. Moreover, combined treatment with depsipeptide and rIGFBP-3 completely suppressed tumor growth and increased the apoptosis rate in vivo in H1299 NSCLC xenografts. Evidence suggests that HDAC inhibitors increased the half-life of rIGFBP-3 protein by blocking protein kinase C (PKC)-mediated phosphorylation and degradation of rIGFBP-3. In addition, combined treatment of IGFBP-3 with an HDAC inhibitor facilitates apoptosis through upregulation of rIGFBP-3 stability and Akt signaling inhibition. The ability of HDAC inhibitors to decrease PKC activation may enhance apoptotic activities of rIGFBP-3 in NSCLC cells in vitro and in vivo. These results indicated that combined treatment with HDAC inhibitor and rIGFBP-3 could be an effective treatment strategy for NSCLC and HNSCC with highly activated PKC. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | WILEY-BLACKWELL | - |
dc.relation.isPartOf | INTERNATIONAL JOURNAL OF CANCER | - |
dc.subject | CELL LUNG-CANCER | - |
dc.subject | BREAST EPITHELIAL-CELLS | - |
dc.subject | HEPATOCELLULAR-CARCINOMA | - |
dc.subject | MULTIPROTEIN COMPLEX | - |
dc.subject | SURVIVIN EXPRESSION | - |
dc.subject | SIGNALING PATHWAYS | - |
dc.subject | DOWN-REGULATION | - |
dc.subject | FACTOR RECEPTOR | - |
dc.subject | KINASE-C | - |
dc.subject | KAPPA-B | - |
dc.title | Histone deacetylase inhibitors enhance the apoptotic activity of insulin-like growth factor binding protein-3 by blocking PKC-induced IGFBP-3 degradation | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000309185300006 | - |
dc.identifier.doi | 10.1002/ijc.27509 | - |
dc.identifier.bibliographicCitation | INTERNATIONAL JOURNAL OF CANCER, v.131, no.10, pp.2253 - 2263 | - |
dc.identifier.scopusid | 2-s2.0-84867033832 | - |
dc.citation.endPage | 2263 | - |
dc.citation.startPage | 2253 | - |
dc.citation.title | INTERNATIONAL JOURNAL OF CANCER | - |
dc.citation.volume | 131 | - |
dc.citation.number | 10 | - |
dc.contributor.affiliatedAuthor | Oh, Seung Hyun | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | Non-small cell lung cancer | - |
dc.subject.keywordAuthor | insulin-like growth factor binding protein-3 | - |
dc.subject.keywordAuthor | head and neck squamous cell carcinoma | - |
dc.subject.keywordAuthor | Akt | - |
dc.subject.keywordAuthor | histone deacetylases | - |
dc.subject.keywordAuthor | protein kinase C | - |
dc.subject.keywordPlus | CELL LUNG-CANCER | - |
dc.subject.keywordPlus | BREAST EPITHELIAL-CELLS | - |
dc.subject.keywordPlus | HEPATOCELLULAR-CARCINOMA | - |
dc.subject.keywordPlus | MULTIPROTEIN COMPLEX | - |
dc.subject.keywordPlus | SURVIVIN EXPRESSION | - |
dc.subject.keywordPlus | SIGNALING PATHWAYS | - |
dc.subject.keywordPlus | DOWN-REGULATION | - |
dc.subject.keywordPlus | FACTOR RECEPTOR | - |
dc.subject.keywordPlus | KINASE-C | - |
dc.subject.keywordPlus | KAPPA-B | - |
dc.relation.journalResearchArea | Oncology | - |
dc.relation.journalWebOfScienceCategory | Oncology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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