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dc.contributor.authorHsu, Hsi-Hsienen_US
dc.contributor.authorCheng, Li-Haoen_US
dc.contributor.authorHo, Tsung-Jungen_US
dc.contributor.authorKuo, Wei-Wenen_US
dc.contributor.authorLin, Yueh-Minen_US
dc.contributor.authorChen, Ming-Chengen_US
dc.contributor.authorLee, Nien-Hungen_US
dc.contributor.authorTsai, Fuu-Jenen_US
dc.contributor.authorTsai, Kun-Hsien_US
dc.contributor.authorHuang, Chih-Yangen_US
dc.date.accessioned2014-12-08T15:35:10Z-
dc.date.available2014-12-08T15:35:10Z-
dc.date.issued2014-01-01en_US
dc.identifier.issn1010-4283en_US
dc.identifier.urihttp://dx.doi.org/10.1007/s13277-013-1041-3en_US
dc.identifier.urihttp://hdl.handle.net/11536/23863-
dc.description.abstractDespite rapid advances in the diagnostic and surgical procedures, hepatocellular carcinoma (HCC) remains one of the most difficult human malignancies to treat. This may be due to the chemoresistant behaviors of HCC. It is believed that acquired resistance could be overcome and improve the overall survival of HCC patients by understanding the mechanisms of chemoresistance in HCC. A stable HA22T cancer line, which is chronically resistant to a histone deacetylase inhibitor, was established. After comparing the molecular mechanism of apicidin-R HA22T cells to parental ones by Western blotting, cell cycle-regulated proteins did not change in apicidin-R cells, but apicidin-R cells were more proliferative and had higher tumor growth (wound-healing assay and nude mice xenograft model). Moreover, apicidin-R cells displayed increased levels of p-IGF-IR, p-PI3K, p-Akt, Bcl-xL, and Bcl-2 but also significantly inhibited the tumor suppressor PTEN protein and apoptotic pathways when compared to the parental strain. Therefore, the highly proliferative effect of apicidin-R HA22T cells was blocked by Akt knockdown. For all these findings, we believe that novel strategies to attenuate IGF-IR/PI3K/Akt signaling could overcome chemoresistance toward the improvement of overall survival of HCC patients.en_US
dc.language.isoen_USen_US
dc.subjectApicidin HA22Ten_US
dc.subjectHepatocellular carcinoma cellsen_US
dc.subjectIGF-IRen_US
dc.subjectPI3Ken_US
dc.subjectAkten_US
dc.titleApicidin-resistant HA22T hepatocellular carcinoma cells massively promote pro-survival capability via IGF-IR/PI3K/Akt signaling pathway activationen_US
dc.typeArticleen_US
dc.identifier.doi10.1007/s13277-013-1041-3en_US
dc.identifier.journalTUMOR BIOLOGYen_US
dc.citation.volume35en_US
dc.citation.issue1en_US
dc.citation.spage303en_US
dc.citation.epage313en_US
dc.contributor.department生物科技學系zh_TW
dc.contributor.departmentDepartment of Biological Science and Technologyen_US
dc.identifier.wosnumberWOS:000331091000039-
dc.citation.woscount2-
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