Hepatic Artery Embolization Induces the Local Overexpression of Transforming Growth Factor β1 in a Rat Hepatoma Model
Introduction: The underlying mechanism involved in the recurrence of hepatoma after hepatic arterial embolization (HAE) is not adequately examined. An immunosuppressive cytokine, transforming growth factor β1 (TGF-β1), can lead to tumor progression and is affected by hypoxia in various cancers. The...
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| Veröffentlicht in: | Liver cancer (Basel ) 2020-01, Vol.9 (1), p.63-72 |
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| creator | Ueshima, Eisuke Nishiofuku, Hideyuki Takaki, Haruyuki Hirata, Yutaka Kodama, Hiroshi Tanaka, Toshihiro Kichikawa, Kimihiko Yamakado, Koichiro Okada, Takuya Sofue, Keitaro Yamaguchi, Masato Sugimoto, Koji Murakami, Takamichi |
| description | Introduction: The underlying mechanism involved in the recurrence of hepatoma after hepatic arterial embolization (HAE) is not adequately examined. An immunosuppressive cytokine, transforming growth factor β1 (TGF-β1), can lead to tumor progression and is affected by hypoxia in various cancers. The study aimed to assess the effect of HAE on the expression of TGF-β1 in a rat hepatoma model. Methods: Sprague-Dawley rats bearing N1S1 hepatoma cells underwent HAE (HAE group, n = 5) or sham treatment (sham group, n = 4). The animals were euthanized at 48 h, and liver tissues were harvested. Immunohistochemistry (IHC) and quantitative polymerase chain reaction (qPCR) were performed to compare the expression of TGF-β1 and hypoxia-inducible factor 1α (HIF-1α) between the HAE and sham groups. In vitro experiments with the N1S1 cell line were also performed under normoxic (21% O 2 ) or hypoxic (1% O 2 ) conditions for 48 h, and the expression of TGF-β1 and HIF-1α was assessed with western blotting and enzyme-linked immunosorbent assay. Statistical data comparisons were performed by Student t test. Results: IHC showed that both the TGF-β1-positive and HIF-1α-positive tumor peripheral areas were larger in the HAE group (6.59 ± 2.49 and 10.26 ± 4.14%; p < 0.001, respectively) than in the sham group (0.34 ± 0.41 and 0.40 ± 0.84% respectively). Similarly, qPCR showed that the mRNA expression levels of TGF-β1 and HIF-1α were higher (1.95 ± 0.38-fold and 1.62 ± 0.37-fold; p < 0.001 and p = 0.002, respectively) in the HAE group than those in the sham group. TGF-β1 expression was suppressed when HIF-1α inhibitors were added (p = 0.001), and HIF-1α expression was upregulated when exogenous TGF-β1 was added (p = 0.033) in N1S1 cells. Conclusion: HAE enhanced local TGF-β1 expression in a rat hepatoma model. In vitro experiments suggest that HAE-induced hypoxic stress may trigger the interdependent expression of TGF-β1 and HIF-1α. |
| doi_str_mv | 10.1159/000502774 |
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An immunosuppressive cytokine, transforming growth factor β1 (TGF-β1), can lead to tumor progression and is affected by hypoxia in various cancers. The study aimed to assess the effect of HAE on the expression of TGF-β1 in a rat hepatoma model. Methods: Sprague-Dawley rats bearing N1S1 hepatoma cells underwent HAE (HAE group, n = 5) or sham treatment (sham group, n = 4). The animals were euthanized at 48 h, and liver tissues were harvested. Immunohistochemistry (IHC) and quantitative polymerase chain reaction (qPCR) were performed to compare the expression of TGF-β1 and hypoxia-inducible factor 1α (HIF-1α) between the HAE and sham groups. In vitro experiments with the N1S1 cell line were also performed under normoxic (21% O 2 ) or hypoxic (1% O 2 ) conditions for 48 h, and the expression of TGF-β1 and HIF-1α was assessed with western blotting and enzyme-linked immunosorbent assay. Statistical data comparisons were performed by Student t test. Results: IHC showed that both the TGF-β1-positive and HIF-1α-positive tumor peripheral areas were larger in the HAE group (6.59 ± 2.49 and 10.26 ± 4.14%; p < 0.001, respectively) than in the sham group (0.34 ± 0.41 and 0.40 ± 0.84% respectively). Similarly, qPCR showed that the mRNA expression levels of TGF-β1 and HIF-1α were higher (1.95 ± 0.38-fold and 1.62 ± 0.37-fold; p < 0.001 and p = 0.002, respectively) in the HAE group than those in the sham group. TGF-β1 expression was suppressed when HIF-1α inhibitors were added (p = 0.001), and HIF-1α expression was upregulated when exogenous TGF-β1 was added (p = 0.033) in N1S1 cells. Conclusion: HAE enhanced local TGF-β1 expression in a rat hepatoma model. In vitro experiments suggest that HAE-induced hypoxic stress may trigger the interdependent expression of TGF-β1 and HIF-1α.</description><identifier>ISSN: 2235-1795</identifier><identifier>EISSN: 1664-5553</identifier><identifier>DOI: 10.1159/000502774</identifier><identifier>PMID: 32071910</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Antibodies ; Cancer ; Carotid arteries ; Catheters ; Collagen ; Cytokines ; Embolization ; Gene expression ; Growth factors ; Hypoxia ; Liver ; Liver cancer ; Medical prognosis ; Original Paper ; Skin ; Tumors ; Veins & arteries</subject><ispartof>Liver cancer (Basel ), 2020-01, Vol.9 (1), p.63-72</ispartof><rights>2019 The Author(s) Published by S. Karger AG, Basel</rights><rights>Copyright © 2019 by S. Karger AG, Basel.</rights><rights>2019 The Author(s) Published by S. Karger AG, Basel . This work is licensed under the Creative Commons Attribution – Non-Commercial – No Derivatives License http://creativecommons.org/licenses/by-nc-nd/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Copyright © 2019 by S. Karger AG, Basel 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c562t-be99dc7a7174ca85f1385a80fd53e0a7d22d9ce8da43de7967ffe2948df1fdcc3</citedby><cites>FETCH-LOGICAL-c562t-be99dc7a7174ca85f1385a80fd53e0a7d22d9ce8da43de7967ffe2948df1fdcc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7024851/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7024851/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27612,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32071910$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ueshima, Eisuke</creatorcontrib><creatorcontrib>Nishiofuku, Hideyuki</creatorcontrib><creatorcontrib>Takaki, Haruyuki</creatorcontrib><creatorcontrib>Hirata, Yutaka</creatorcontrib><creatorcontrib>Kodama, Hiroshi</creatorcontrib><creatorcontrib>Tanaka, Toshihiro</creatorcontrib><creatorcontrib>Kichikawa, Kimihiko</creatorcontrib><creatorcontrib>Yamakado, Koichiro</creatorcontrib><creatorcontrib>Okada, Takuya</creatorcontrib><creatorcontrib>Sofue, Keitaro</creatorcontrib><creatorcontrib>Yamaguchi, Masato</creatorcontrib><creatorcontrib>Sugimoto, Koji</creatorcontrib><creatorcontrib>Murakami, Takamichi</creatorcontrib><title>Hepatic Artery Embolization Induces the Local Overexpression of Transforming Growth Factor β1 in a Rat Hepatoma Model</title><title>Liver cancer (Basel )</title><addtitle>Liver Cancer</addtitle><description>Introduction: The underlying mechanism involved in the recurrence of hepatoma after hepatic arterial embolization (HAE) is not adequately examined. An immunosuppressive cytokine, transforming growth factor β1 (TGF-β1), can lead to tumor progression and is affected by hypoxia in various cancers. The study aimed to assess the effect of HAE on the expression of TGF-β1 in a rat hepatoma model. Methods: Sprague-Dawley rats bearing N1S1 hepatoma cells underwent HAE (HAE group, n = 5) or sham treatment (sham group, n = 4). The animals were euthanized at 48 h, and liver tissues were harvested. Immunohistochemistry (IHC) and quantitative polymerase chain reaction (qPCR) were performed to compare the expression of TGF-β1 and hypoxia-inducible factor 1α (HIF-1α) between the HAE and sham groups. In vitro experiments with the N1S1 cell line were also performed under normoxic (21% O 2 ) or hypoxic (1% O 2 ) conditions for 48 h, and the expression of TGF-β1 and HIF-1α was assessed with western blotting and enzyme-linked immunosorbent assay. Statistical data comparisons were performed by Student t test. Results: IHC showed that both the TGF-β1-positive and HIF-1α-positive tumor peripheral areas were larger in the HAE group (6.59 ± 2.49 and 10.26 ± 4.14%; p < 0.001, respectively) than in the sham group (0.34 ± 0.41 and 0.40 ± 0.84% respectively). Similarly, qPCR showed that the mRNA expression levels of TGF-β1 and HIF-1α were higher (1.95 ± 0.38-fold and 1.62 ± 0.37-fold; p < 0.001 and p = 0.002, respectively) in the HAE group than those in the sham group. TGF-β1 expression was suppressed when HIF-1α inhibitors were added (p = 0.001), and HIF-1α expression was upregulated when exogenous TGF-β1 was added (p = 0.033) in N1S1 cells. Conclusion: HAE enhanced local TGF-β1 expression in a rat hepatoma model. In vitro experiments suggest that HAE-induced hypoxic stress may trigger the interdependent expression of TGF-β1 and HIF-1α.</description><subject>Antibodies</subject><subject>Cancer</subject><subject>Carotid arteries</subject><subject>Catheters</subject><subject>Collagen</subject><subject>Cytokines</subject><subject>Embolization</subject><subject>Gene expression</subject><subject>Growth factors</subject><subject>Hypoxia</subject><subject>Liver</subject><subject>Liver cancer</subject><subject>Medical prognosis</subject><subject>Original Paper</subject><subject>Skin</subject><subject>Tumors</subject><subject>Veins & arteries</subject><issn>2235-1795</issn><issn>1664-5553</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>BENPR</sourceid><recordid>eNptkc2O0zAUhS0EYqphFuwRssQGFgHbiWN7gzSq5qdS0UhoWFuufd1mSOJgO4XhsXgQnomUlvIjVlfy_XTOuT4IPaXkNaVcvSGEcMKEqB6gGa3rquCclw_RjLGSF1QofoLOUrqbMCIJEUo8RiclI4IqSmZoew2DyY3F5zFDvMcX3Sq0zdfpKfR40bvRQsJ5A3gZrGnxzRYifBkipLQDgse30fTJh9g1_RpfxfA5b_ClsTlE_P0bxU2PDX5vMv7pEzqD3wUH7RP0yJs2wdlhnqIPlxe38-tieXO1mJ8vC8trlosVKOWsMIKKyhrJPS0lN5J4x0sgRjjGnLIgnalKB0LVwntgqpLOU--sLU_R273uMK46cBb6HE2rh9h0Jt7rYBr996ZvNnodtloQVklOJ4GXB4EYPo2Qsu6aZKFtTQ9hTHr6ZMkFl3SHvvgHvQtj7KfzNOP1FFxUspqoV3vKxpBSBH8MQ4neFaqPhU7s8z_TH8lf9f22_GjiGuIRWC7mewk9OD9Rz_5LHVx-ANcGsi4</recordid><startdate>20200101</startdate><enddate>20200101</enddate><creator>Ueshima, Eisuke</creator><creator>Nishiofuku, Hideyuki</creator><creator>Takaki, Haruyuki</creator><creator>Hirata, Yutaka</creator><creator>Kodama, Hiroshi</creator><creator>Tanaka, Toshihiro</creator><creator>Kichikawa, Kimihiko</creator><creator>Yamakado, Koichiro</creator><creator>Okada, Takuya</creator><creator>Sofue, Keitaro</creator><creator>Yamaguchi, Masato</creator><creator>Sugimoto, Koji</creator><creator>Murakami, Takamichi</creator><general>S. Karger AG</general><scope>M--</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>NAPCQ</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PIMPY</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20200101</creationdate><title>Hepatic Artery Embolization Induces the Local Overexpression of Transforming Growth Factor β1 in a Rat Hepatoma Model</title><author>Ueshima, Eisuke ; Nishiofuku, Hideyuki ; Takaki, Haruyuki ; Hirata, Yutaka ; Kodama, Hiroshi ; Tanaka, Toshihiro ; Kichikawa, Kimihiko ; Yamakado, Koichiro ; Okada, Takuya ; Sofue, Keitaro ; Yamaguchi, Masato ; Sugimoto, Koji ; Murakami, Takamichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c562t-be99dc7a7174ca85f1385a80fd53e0a7d22d9ce8da43de7967ffe2948df1fdcc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Antibodies</topic><topic>Cancer</topic><topic>Carotid arteries</topic><topic>Catheters</topic><topic>Collagen</topic><topic>Cytokines</topic><topic>Embolization</topic><topic>Gene expression</topic><topic>Growth factors</topic><topic>Hypoxia</topic><topic>Liver</topic><topic>Liver cancer</topic><topic>Medical prognosis</topic><topic>Original Paper</topic><topic>Skin</topic><topic>Tumors</topic><topic>Veins & arteries</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ueshima, Eisuke</creatorcontrib><creatorcontrib>Nishiofuku, Hideyuki</creatorcontrib><creatorcontrib>Takaki, Haruyuki</creatorcontrib><creatorcontrib>Hirata, Yutaka</creatorcontrib><creatorcontrib>Kodama, Hiroshi</creatorcontrib><creatorcontrib>Tanaka, Toshihiro</creatorcontrib><creatorcontrib>Kichikawa, Kimihiko</creatorcontrib><creatorcontrib>Yamakado, Koichiro</creatorcontrib><creatorcontrib>Okada, Takuya</creatorcontrib><creatorcontrib>Sofue, Keitaro</creatorcontrib><creatorcontrib>Yamaguchi, Masato</creatorcontrib><creatorcontrib>Sugimoto, Koji</creatorcontrib><creatorcontrib>Murakami, Takamichi</creatorcontrib><collection>Karger Open Access</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Liver cancer (Basel )</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ueshima, Eisuke</au><au>Nishiofuku, Hideyuki</au><au>Takaki, Haruyuki</au><au>Hirata, Yutaka</au><au>Kodama, Hiroshi</au><au>Tanaka, Toshihiro</au><au>Kichikawa, Kimihiko</au><au>Yamakado, Koichiro</au><au>Okada, Takuya</au><au>Sofue, Keitaro</au><au>Yamaguchi, Masato</au><au>Sugimoto, Koji</au><au>Murakami, Takamichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hepatic Artery Embolization Induces the Local Overexpression of Transforming Growth Factor β1 in a Rat Hepatoma Model</atitle><jtitle>Liver cancer (Basel )</jtitle><addtitle>Liver Cancer</addtitle><date>2020-01-01</date><risdate>2020</risdate><volume>9</volume><issue>1</issue><spage>63</spage><epage>72</epage><pages>63-72</pages><issn>2235-1795</issn><eissn>1664-5553</eissn><abstract>Introduction: The underlying mechanism involved in the recurrence of hepatoma after hepatic arterial embolization (HAE) is not adequately examined. An immunosuppressive cytokine, transforming growth factor β1 (TGF-β1), can lead to tumor progression and is affected by hypoxia in various cancers. The study aimed to assess the effect of HAE on the expression of TGF-β1 in a rat hepatoma model. Methods: Sprague-Dawley rats bearing N1S1 hepatoma cells underwent HAE (HAE group, n = 5) or sham treatment (sham group, n = 4). The animals were euthanized at 48 h, and liver tissues were harvested. Immunohistochemistry (IHC) and quantitative polymerase chain reaction (qPCR) were performed to compare the expression of TGF-β1 and hypoxia-inducible factor 1α (HIF-1α) between the HAE and sham groups. In vitro experiments with the N1S1 cell line were also performed under normoxic (21% O 2 ) or hypoxic (1% O 2 ) conditions for 48 h, and the expression of TGF-β1 and HIF-1α was assessed with western blotting and enzyme-linked immunosorbent assay. Statistical data comparisons were performed by Student t test. Results: IHC showed that both the TGF-β1-positive and HIF-1α-positive tumor peripheral areas were larger in the HAE group (6.59 ± 2.49 and 10.26 ± 4.14%; p < 0.001, respectively) than in the sham group (0.34 ± 0.41 and 0.40 ± 0.84% respectively). Similarly, qPCR showed that the mRNA expression levels of TGF-β1 and HIF-1α were higher (1.95 ± 0.38-fold and 1.62 ± 0.37-fold; p < 0.001 and p = 0.002, respectively) in the HAE group than those in the sham group. TGF-β1 expression was suppressed when HIF-1α inhibitors were added (p = 0.001), and HIF-1α expression was upregulated when exogenous TGF-β1 was added (p = 0.033) in N1S1 cells. Conclusion: HAE enhanced local TGF-β1 expression in a rat hepatoma model. In vitro experiments suggest that HAE-induced hypoxic stress may trigger the interdependent expression of TGF-β1 and HIF-1α.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>32071910</pmid><doi>10.1159/000502774</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Antibodies Cancer Carotid arteries Catheters Collagen Cytokines Embolization Gene expression Growth factors Hypoxia Liver Liver cancer Medical prognosis Original Paper Skin Tumors Veins & arteries |
| title | Hepatic Artery Embolization Induces the Local Overexpression of Transforming Growth Factor β1 in a Rat Hepatoma Model |
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