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dc.contributor.authorChou, Yu-Tingen_US
dc.contributor.authorChen, Li-Yangen_US
dc.contributor.authorTsai, Shin-Linen_US
dc.contributor.authorTu, Hsiao-Chenen_US
dc.contributor.authorLu, Jeng-Weien_US
dc.contributor.authorCiou, Shih-Cien_US
dc.contributor.authorWang, Horng-Daren_US
dc.contributor.authorYuh, Chiou-Hwaen_US
dc.date.accessioned2019-08-02T02:15:31Z-
dc.date.available2019-08-02T02:15:31Z-
dc.date.issued2019-03-01en_US
dc.identifier.issn0143-3334en_US
dc.identifier.urihttp://dx.doi.org/10.1093/carcin/bgy155en_US
dc.identifier.urihttp://hdl.handle.net/11536/152214-
dc.description.abstractDysregulation of the enzymes involved in the pentose phosphate pathway (PPP) is known to promote tumorigenesis. Our recent study demonstrated that ribose-5-phosphate isomerase (RPIA), a key regulator of the PPP, regulates hepatoma cell proliferation and colony formation. Our studies in zebrafish reveal that RPIA-mediated hepatocarcinogenesis requires extracellular signal-regulated kinase (ERK) and beta-catenin signaling. To further investigate RPIA-mediated hepatocarcinogenesis, two independent lines of transgenic zebrafish expressing human RPIA in the liver were generated. These studies reveal that RPIA overexpression triggers lipogenic factor/enzyme expression, steatosis, fibrosis and proliferation of the liver. In addition, the severity of fibrosis and the extent of proliferation are positively correlated with RPIA expression levels. Furthermore, RPIA-mediated induction of hepatocellular carcinoma (HCC) requires the ERK and beta-catenin signaling pathway but is not dependent upon transaldolase levels. Our study presents a mechanism for RPIA-mediated hepatocarcinogenesis and suggests that RPIA represents a valuable therapeutic target for the treatment of HCC.en_US
dc.language.isoen_USen_US
dc.titleRibose-5-phosphate isomerase A overexpression promotes liver cancer development in transgenic zebrafish via activation of ERK and beta-catenin pathwaysen_US
dc.typeArticleen_US
dc.identifier.doi10.1093/carcin/bgy155en_US
dc.identifier.journalCARCINOGENESISen_US
dc.citation.volume40en_US
dc.citation.issue3en_US
dc.citation.spage461en_US
dc.citation.epage473en_US
dc.contributor.department生物科技學系zh_TW
dc.contributor.departmentDepartment of Biological Science and Technologyen_US
dc.identifier.wosnumberWOS:000472794100008en_US
dc.citation.woscount1en_US
Appears in Collections:Articles