Inhibition of Hepatic Stellate Cell Activation Suppresses Tumorigenicity of Hepatocellular Carcinoma in Mice
DC Field | Value | Language |
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dc.contributor.author | Kang, Min-Jung | - |
dc.contributor.author | Lee, Soovin | - |
dc.contributor.author | Jung, Usuk | - |
dc.contributor.author | Mandal, Chanchal | - |
dc.contributor.author | Park, Heekyung | - |
dc.contributor.author | Stetler-Stevenson, William G. | - |
dc.contributor.author | Kim, Young-Sik | - |
dc.contributor.author | Moon, Ji Wook | - |
dc.contributor.author | Park, Sun-Hwa | - |
dc.contributor.author | Oh, Junseo | - |
dc.date.accessioned | 2022-02-13T14:41:05Z | - |
dc.date.available | 2022-02-13T14:41:05Z | - |
dc.date.created | 2022-01-19 | - |
dc.date.issued | 2021-12 | - |
dc.identifier.issn | 0002-9440 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/135633 | - |
dc.description.abstract | Transdifferentiation (or activation) of hepatic stellate cells (HSCs) to myofibroblasts is a key event in liver fibrosis. Activated HSCs in the tumor microenvironment reportedly promote tumor progression. This study analyzed the effect of an inhibitor of HSC activation, retinol-binding protein-albumin domain III fusion protein (R-III), on protumorigenic functions of HSCs. Although conditioned medium collected from activated HSCs enhanced the migration, invasion, and proliferation of the hepatocellular carcinoma cell line Hepa-1c1c7, this effect was not observed in Hepa-1c1c7 cells treated with conditioned medium from R-III-exposed HSCs. In a subcutaneous tumor model, larger tumors with increased vascular density were formed in mice transplanted with Hepa-1c1c7+HSC than in mice transplanted with Hepa-1c1c7 cells alone. Intriguingly, when Hepa-1c1c7+HSC-transplanted mice were injected intravenously with R-III, a reduction in vascular density and extended tumor necrosis were observed. In an orthotopic tumor model, co-transplantation of HSCs enhanced tumor growth, angiogenesis, and regional metastasis accompanied by increased peritumoral lymphatic vessel density, which was abolished by R-III. In vitro study showed that R-III treatment affected the synthesis of pro-angiogenic and anti-angiogenic factors in activated HSCs, which might be the potential mechanism underlying the R-III effect. These findings suggest that the inhibition of HSC activation abrogates HSC-induced tumor angiogenesis and growth, which represents an attractive therapeutic strategy. (Am J Pathol 2021, 191: 2219-2230; https://doi.org/10.1016/j.ajpath.2021.08.004) | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | ELSEVIER SCIENCE INC | - |
dc.subject | RETINOL-BINDING-PROTEIN | - |
dc.subject | VEGF-D PROMOTES | - |
dc.subject | MOUSE MODEL | - |
dc.subject | FUSION PROTEIN | - |
dc.subject | ANGIOGENESIS | - |
dc.subject | GROWTH | - |
dc.subject | LIPOCYTES | - |
dc.subject | FIBROSIS | - |
dc.subject | PARTNERS | - |
dc.subject | SPREAD | - |
dc.title | Inhibition of Hepatic Stellate Cell Activation Suppresses Tumorigenicity of Hepatocellular Carcinoma in Mice | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Kim, Young-Sik | - |
dc.contributor.affiliatedAuthor | Oh, Junseo | - |
dc.identifier.doi | 10.1016/j.ajpath.2021.08.004 | - |
dc.identifier.scopusid | 2-s2.0-85119252183 | - |
dc.identifier.wosid | 000721488300003 | - |
dc.identifier.bibliographicCitation | AMERICAN JOURNAL OF PATHOLOGY, v.191, no.12, pp.2219 - 2230 | - |
dc.relation.isPartOf | AMERICAN JOURNAL OF PATHOLOGY | - |
dc.citation.title | AMERICAN JOURNAL OF PATHOLOGY | - |
dc.citation.volume | 191 | - |
dc.citation.number | 12 | - |
dc.citation.startPage | 2219 | - |
dc.citation.endPage | 2230 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Pathology | - |
dc.relation.journalWebOfScienceCategory | Pathology | - |
dc.subject.keywordPlus | ANGIOGENESIS | - |
dc.subject.keywordPlus | FIBROSIS | - |
dc.subject.keywordPlus | FUSION PROTEIN | - |
dc.subject.keywordPlus | GROWTH | - |
dc.subject.keywordPlus | LIPOCYTES | - |
dc.subject.keywordPlus | MOUSE MODEL | - |
dc.subject.keywordPlus | PARTNERS | - |
dc.subject.keywordPlus | RETINOL-BINDING-PROTEIN | - |
dc.subject.keywordPlus | SPREAD | - |
dc.subject.keywordPlus | VEGF-D PROMOTES | - |
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