Hyaluronic acid inhibition by 4-methylumbelliferone reduces the expression of cancer stem cells markers during hepatocarcinogenesis
Hyaluronic acid (HA) is a glycosaminoglycan of extracellular matrix related to cell surface which interacts with various cell types. To understand the role of HA during hepatocarcinogenesis, we assessed the effect of the inhibition of HA deposition and its association with heterogeneous hepatocellul...
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| description | Hyaluronic acid (HA) is a glycosaminoglycan of extracellular matrix related to cell surface which interacts with various cell types. To understand the role of HA during hepatocarcinogenesis, we assessed the effect of the inhibition of HA deposition and its association with heterogeneous hepatocellular carcinoma (HCC) cells. In this study, we used transgenic mice C57BL/6J-Tg(Alb1HBV)44Bri/J (HBV-TG) and normal C57BL/6 J (WT) for
in vivo
study, while HCC cells Huh7 and JHH6 as
in vitro
models. Both models were treated with an HA inhibitor 4-methylumbelliferone (4MU). We observed that 4MU treatments in animal model down-regulated the mRNA expressions of HA-related genes Has3 and Hyal2 only in HBV-TG but not in normal WT. As observed
in vivo
, in HCC cell lines, the HAS2 mRNA expression was down-regulated in Huh7 while HAS3 in JHH6, both with or without the presence of extrinsic HA. Interestingly, in both models, the expressions of various cancer stem cells (CD44, CD90, CD133, and EpCAM) were also decreased. Further, histological analysis showed that 4MU treatment with dose 25 mg/kg/day reduced fibrosis, inflammation, and steatosis
in vivo
, in addition to be pro-apoptotic. We concluded that the inhibition of HA reduced the expressions of HA-related genes and stem cells markers in both models, indicating a possible modulation of cells-to-cells and cells-to-matrix interaction. |
| doi_str_mv | 10.1038/s41598-019-40436-6 |
| format | Article |
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in vivo
study, while HCC cells Huh7 and JHH6 as
in vitro
models. Both models were treated with an HA inhibitor 4-methylumbelliferone (4MU). We observed that 4MU treatments in animal model down-regulated the mRNA expressions of HA-related genes Has3 and Hyal2 only in HBV-TG but not in normal WT. As observed
in vivo
, in HCC cell lines, the HAS2 mRNA expression was down-regulated in Huh7 while HAS3 in JHH6, both with or without the presence of extrinsic HA. Interestingly, in both models, the expressions of various cancer stem cells (CD44, CD90, CD133, and EpCAM) were also decreased. Further, histological analysis showed that 4MU treatment with dose 25 mg/kg/day reduced fibrosis, inflammation, and steatosis
in vivo
, in addition to be pro-apoptotic. We concluded that the inhibition of HA reduced the expressions of HA-related genes and stem cells markers in both models, indicating a possible modulation of cells-to-cells and cells-to-matrix interaction.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-019-40436-6</identifier><identifier>PMID: 30858465</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/100 ; 13/31 ; 13/51 ; 13/56 ; 14/63 ; 38/1 ; 38/77 ; 631/67/1504/1610 ; 631/67/71 ; 64/110 ; 64/60 ; 82/80 ; Animal models ; Animals ; Apoptosis ; Biomarkers, Tumor - metabolism ; Carcinogenesis - drug effects ; Carcinogenesis - metabolism ; Carcinoma, Hepatocellular - metabolism ; CD44 antigen ; CD90 antigen ; Cell Line, Tumor ; Cell surface ; Extracellular matrix ; Fibrosis ; Gene expression ; Hepatocellular carcinoma ; Humanities and Social Sciences ; Humans ; Hyaluronic acid ; Hyaluronic Acid - antagonists & inhibitors ; Hymecromone - pharmacology ; Liver cancer ; Liver Neoplasms, Experimental - metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; multidisciplinary ; Neoplastic Stem Cells - metabolism ; Neoplastic Stem Cells - pathology ; Science ; Science (multidisciplinary) ; Steatosis ; Stem cell transplantation ; Stem cells ; Transgenic mice</subject><ispartof>Scientific reports, 2019-03, Vol.9 (1), p.4026, Article 4026</ispartof><rights>The Author(s) 2019</rights><rights>This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c577t-d393f943173fc19c6548abb917e056856657772f00cce69b4c3a6cc3438c99dc3</citedby><cites>FETCH-LOGICAL-c577t-d393f943173fc19c6548abb917e056856657772f00cce69b4c3a6cc3438c99dc3</cites><orcidid>0000-0001-9699-7578 ; 0000-0001-7819-6830 ; 0000-0001-6596-7595</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6411988/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6411988/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30858465$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sukowati, Caecilia H. C.</creatorcontrib><creatorcontrib>Anfuso, Beatrice</creatorcontrib><creatorcontrib>Fiore, Esteban</creatorcontrib><creatorcontrib>Ie, Susan I.</creatorcontrib><creatorcontrib>Raseni, Alan</creatorcontrib><creatorcontrib>Vascotto, Fulvia</creatorcontrib><creatorcontrib>Avellini, Claudio</creatorcontrib><creatorcontrib>Mazzolini, Guillermo</creatorcontrib><creatorcontrib>Tiribelli, Claudio</creatorcontrib><title>Hyaluronic acid inhibition by 4-methylumbelliferone reduces the expression of cancer stem cells markers during hepatocarcinogenesis</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Hyaluronic acid (HA) is a glycosaminoglycan of extracellular matrix related to cell surface which interacts with various cell types. To understand the role of HA during hepatocarcinogenesis, we assessed the effect of the inhibition of HA deposition and its association with heterogeneous hepatocellular carcinoma (HCC) cells. In this study, we used transgenic mice C57BL/6J-Tg(Alb1HBV)44Bri/J (HBV-TG) and normal C57BL/6 J (WT) for
in vivo
study, while HCC cells Huh7 and JHH6 as
in vitro
models. Both models were treated with an HA inhibitor 4-methylumbelliferone (4MU). We observed that 4MU treatments in animal model down-regulated the mRNA expressions of HA-related genes Has3 and Hyal2 only in HBV-TG but not in normal WT. As observed
in vivo
, in HCC cell lines, the HAS2 mRNA expression was down-regulated in Huh7 while HAS3 in JHH6, both with or without the presence of extrinsic HA. Interestingly, in both models, the expressions of various cancer stem cells (CD44, CD90, CD133, and EpCAM) were also decreased. Further, histological analysis showed that 4MU treatment with dose 25 mg/kg/day reduced fibrosis, inflammation, and steatosis
in vivo
, in addition to be pro-apoptotic. We concluded that the inhibition of HA reduced the expressions of HA-related genes and stem cells markers in both models, indicating a possible modulation of cells-to-cells and cells-to-matrix interaction.</description><subject>13/100</subject><subject>13/31</subject><subject>13/51</subject><subject>13/56</subject><subject>14/63</subject><subject>38/1</subject><subject>38/77</subject><subject>631/67/1504/1610</subject><subject>631/67/71</subject><subject>64/110</subject><subject>64/60</subject><subject>82/80</subject><subject>Animal models</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Carcinogenesis - drug effects</subject><subject>Carcinogenesis - metabolism</subject><subject>Carcinoma, Hepatocellular - metabolism</subject><subject>CD44 antigen</subject><subject>CD90 antigen</subject><subject>Cell Line, Tumor</subject><subject>Cell surface</subject><subject>Extracellular matrix</subject><subject>Fibrosis</subject><subject>Gene expression</subject><subject>Hepatocellular carcinoma</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Hyaluronic acid</subject><subject>Hyaluronic Acid - antagonists & inhibitors</subject><subject>Hymecromone - pharmacology</subject><subject>Liver cancer</subject><subject>Liver Neoplasms, Experimental - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>multidisciplinary</subject><subject>Neoplastic Stem Cells - metabolism</subject><subject>Neoplastic Stem Cells - pathology</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Steatosis</subject><subject>Stem cell transplantation</subject><subject>Stem cells</subject><subject>Transgenic mice</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kc1u1TAQhaMK1FalL8ACWWId8H_iDRKqoEWqxAbWljOZ3LgkdrATxF3z4vXlllI2eGNL850zRz5V9ZLRN4yK9m2WTJm2pszUkkqha31SnXMqVc0F58-evM-qy5zvaDmKG8nMaXUmaKtaqdV59etm76YtxeCBOPA98WH0nV99DKTbE1nPuI77aZs7nCY_YCGRJOw3wEzWEQn-XBLmfODjQMAFwETyijOBoshkdukbpkz6LfmwIyMubo3gEvgQdxgw-_yiej64KePlw31Rff344cvVTX37-frT1fvbGlTTrHUvjBiMFKwRAzADWsnWdZ1hDVKlW6V1wRo-UAqA2nQShNMAQooWjOlBXFTvjr7L1s3YA4Y1uckuyZeQexudt_9Ogh_tLv6wWjJm2rYYvH4wSPH7hnm1d3FLoWS2nBnKqBZcFYofKUgx54TD4wZG7aE7e-zOlu7s7-6sLqJXT7M9Sv40VQBxBPJy-EhMf3f_x_YeD2-odw</recordid><startdate>20190311</startdate><enddate>20190311</enddate><creator>Sukowati, Caecilia H. 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C.</creatorcontrib><creatorcontrib>Anfuso, Beatrice</creatorcontrib><creatorcontrib>Fiore, Esteban</creatorcontrib><creatorcontrib>Ie, Susan I.</creatorcontrib><creatorcontrib>Raseni, Alan</creatorcontrib><creatorcontrib>Vascotto, Fulvia</creatorcontrib><creatorcontrib>Avellini, Claudio</creatorcontrib><creatorcontrib>Mazzolini, Guillermo</creatorcontrib><creatorcontrib>Tiribelli, Claudio</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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 One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</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 Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</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 Basic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sukowati, Caecilia H. C.</au><au>Anfuso, Beatrice</au><au>Fiore, Esteban</au><au>Ie, Susan I.</au><au>Raseni, Alan</au><au>Vascotto, Fulvia</au><au>Avellini, Claudio</au><au>Mazzolini, Guillermo</au><au>Tiribelli, Claudio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hyaluronic acid inhibition by 4-methylumbelliferone reduces the expression of cancer stem cells markers during hepatocarcinogenesis</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2019-03-11</date><risdate>2019</risdate><volume>9</volume><issue>1</issue><spage>4026</spage><pages>4026-</pages><artnum>4026</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Hyaluronic acid (HA) is a glycosaminoglycan of extracellular matrix related to cell surface which interacts with various cell types. To understand the role of HA during hepatocarcinogenesis, we assessed the effect of the inhibition of HA deposition and its association with heterogeneous hepatocellular carcinoma (HCC) cells. In this study, we used transgenic mice C57BL/6J-Tg(Alb1HBV)44Bri/J (HBV-TG) and normal C57BL/6 J (WT) for
in vivo
study, while HCC cells Huh7 and JHH6 as
in vitro
models. Both models were treated with an HA inhibitor 4-methylumbelliferone (4MU). We observed that 4MU treatments in animal model down-regulated the mRNA expressions of HA-related genes Has3 and Hyal2 only in HBV-TG but not in normal WT. As observed
in vivo
, in HCC cell lines, the HAS2 mRNA expression was down-regulated in Huh7 while HAS3 in JHH6, both with or without the presence of extrinsic HA. Interestingly, in both models, the expressions of various cancer stem cells (CD44, CD90, CD133, and EpCAM) were also decreased. Further, histological analysis showed that 4MU treatment with dose 25 mg/kg/day reduced fibrosis, inflammation, and steatosis
in vivo
, in addition to be pro-apoptotic. We concluded that the inhibition of HA reduced the expressions of HA-related genes and stem cells markers in both models, indicating a possible modulation of cells-to-cells and cells-to-matrix interaction.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>30858465</pmid><doi>10.1038/s41598-019-40436-6</doi><orcidid>https://orcid.org/0000-0001-9699-7578</orcidid><orcidid>https://orcid.org/0000-0001-7819-6830</orcidid><orcidid>https://orcid.org/0000-0001-6596-7595</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 13/100 13/31 13/51 13/56 14/63 38/1 38/77 631/67/1504/1610 631/67/71 64/110 64/60 82/80 Animal models Animals Apoptosis Biomarkers, Tumor - metabolism Carcinogenesis - drug effects Carcinogenesis - metabolism Carcinoma, Hepatocellular - metabolism CD44 antigen CD90 antigen Cell Line, Tumor Cell surface Extracellular matrix Fibrosis Gene expression Hepatocellular carcinoma Humanities and Social Sciences Humans Hyaluronic acid Hyaluronic Acid - antagonists & inhibitors Hymecromone - pharmacology Liver cancer Liver Neoplasms, Experimental - metabolism Male Mice Mice, Inbred C57BL Mice, Transgenic multidisciplinary Neoplastic Stem Cells - metabolism Neoplastic Stem Cells - pathology Science Science (multidisciplinary) Steatosis Stem cell transplantation Stem cells Transgenic mice |
| title | Hyaluronic acid inhibition by 4-methylumbelliferone reduces the expression of cancer stem cells markers during hepatocarcinogenesis |
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