Sulforaphane inhibits TGF-β-induced epithelial-mesenchymal transition of hepatocellular carcinoma cells via the reactive oxygen species-dependent pathway
Sulforaphane is recognized as a safe antitumor agent derived from various cruciferous vegetables, including broccoli. It has been demonstrated that sulforaphase is a potent antitumor agent in diverse cancers. However, its effect on hepatocellular carcinoma remains largely unknown. Here, we show that...
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| Veröffentlicht in: | Oncology reports 2016-05, Vol.35 (5), p.2977-2983 |
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| creator | WU, JINSHENG HAN, JINGLI HOU, BENXIN DENG, CHENGWEI WU, HUANLIANG SHEN, LIANGFANG |
| description | Sulforaphane is recognized as a safe antitumor agent derived from various cruciferous vegetables, including broccoli. It has been demonstrated that sulforaphase is a potent antitumor agent in diverse cancers. However, its effect on hepatocellular carcinoma remains largely unknown. Here, we show that sulforaphane inhibits TGF-β-induced epithelial-mesenchymal transition of hepatocellular carcinoma cell via the reactive oxygen species-dependent pathway. We found sulforaphane inhibited hepatocellular carcinoma cell proliferation in a dose- and time-dependent manner. Sulforaphane induced G0/G1 phase cell cycle arrest and promoted cell apoptosis. A set of experiments showed that sulforaphase inhibited hepatocellular carcinoma cell migration and invasion, inhibited the formation of fibroblast like mesenchymal cells and the expression of Vimentin, but increased the expression of E-cadherin, suggesting sulforaphane suppresses epithelial-mesenchymal transition (EMT) process. Cotreatment with N-acetyl-L-cysteine inhibited sulforaphane-inhibited invasion and upregulation of E-cadherin and almost completely abolished the sulforaphane-induced expression of Vimentin. The effect of sulforaphane on the growth of hepatocellular carcinoma cells was confirmed by a xenograft tumor growth model. All our finding indicated that sulforaphane is a promising and safe strategy for treating hepatocellular carcinoma. |
| doi_str_mv | 10.3892/or.2016.4638 |
| format | Article |
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It has been demonstrated that sulforaphase is a potent antitumor agent in diverse cancers. However, its effect on hepatocellular carcinoma remains largely unknown. Here, we show that sulforaphane inhibits TGF-β-induced epithelial-mesenchymal transition of hepatocellular carcinoma cell via the reactive oxygen species-dependent pathway. We found sulforaphane inhibited hepatocellular carcinoma cell proliferation in a dose- and time-dependent manner. Sulforaphane induced G0/G1 phase cell cycle arrest and promoted cell apoptosis. A set of experiments showed that sulforaphase inhibited hepatocellular carcinoma cell migration and invasion, inhibited the formation of fibroblast like mesenchymal cells and the expression of Vimentin, but increased the expression of E-cadherin, suggesting sulforaphane suppresses epithelial-mesenchymal transition (EMT) process. Cotreatment with N-acetyl-L-cysteine inhibited sulforaphane-inhibited invasion and upregulation of E-cadherin and almost completely abolished the sulforaphane-induced expression of Vimentin. The effect of sulforaphane on the growth of hepatocellular carcinoma cells was confirmed by a xenograft tumor growth model. All our finding indicated that sulforaphane is a promising and safe strategy for treating hepatocellular carcinoma.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2016.4638</identifier><identifier>PMID: 26935987</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Animals ; Antineoplastic Agents - pharmacology ; Apoptosis ; Bladder cancer ; Carcinoma, Hepatocellular - drug therapy ; Carcinoma, Hepatocellular - pathology ; Cell cycle ; Cell growth ; Cell Movement ; Cell Shape - drug effects ; Colorectal cancer ; Development and progression ; epithelial-mesenchymal transition ; Epithelial-Mesenchymal Transition - drug effects ; Female ; G1 Phase Cell Cycle Checkpoints ; Gene expression ; Genetic aspects ; Growth models ; Health aspects ; Hep G2 Cells ; hepatocellular carcinoma ; Hepatoma ; Humans ; Inhibitory Concentration 50 ; Isothiocyanates - pharmacology ; Leukemia ; Liver cancer ; Liver Neoplasms - drug therapy ; Liver Neoplasms - pathology ; Medical prognosis ; Metastasis ; Mice, Inbred BALB C ; Mice, Nude ; Microscopy ; Morphology ; Neoplasm Invasiveness ; Properties ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Studies ; sulforaphane ; Thiocyanates ; Thyroid cancer ; Transforming Growth Factor beta - physiology ; Transforming growth factors ; Xenograft Model Antitumor Assays</subject><ispartof>Oncology reports, 2016-05, Vol.35 (5), p.2977-2983</ispartof><rights>Copyright © 2016, Spandidos Publications</rights><rights>COPYRIGHT 2016 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c486t-2ae34bafff643eef897c0aa30534f7ab892b67afdf9142f11f2859ec6f4759e93</citedby><cites>FETCH-LOGICAL-c486t-2ae34bafff643eef897c0aa30534f7ab892b67afdf9142f11f2859ec6f4759e93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26935987$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>WU, JINSHENG</creatorcontrib><creatorcontrib>HAN, JINGLI</creatorcontrib><creatorcontrib>HOU, BENXIN</creatorcontrib><creatorcontrib>DENG, CHENGWEI</creatorcontrib><creatorcontrib>WU, HUANLIANG</creatorcontrib><creatorcontrib>SHEN, LIANGFANG</creatorcontrib><title>Sulforaphane inhibits TGF-β-induced epithelial-mesenchymal transition of hepatocellular carcinoma cells via the reactive oxygen species-dependent pathway</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>Sulforaphane is recognized as a safe antitumor agent derived from various cruciferous vegetables, including broccoli. It has been demonstrated that sulforaphase is a potent antitumor agent in diverse cancers. However, its effect on hepatocellular carcinoma remains largely unknown. Here, we show that sulforaphane inhibits TGF-β-induced epithelial-mesenchymal transition of hepatocellular carcinoma cell via the reactive oxygen species-dependent pathway. We found sulforaphane inhibited hepatocellular carcinoma cell proliferation in a dose- and time-dependent manner. Sulforaphane induced G0/G1 phase cell cycle arrest and promoted cell apoptosis. A set of experiments showed that sulforaphase inhibited hepatocellular carcinoma cell migration and invasion, inhibited the formation of fibroblast like mesenchymal cells and the expression of Vimentin, but increased the expression of E-cadherin, suggesting sulforaphane suppresses epithelial-mesenchymal transition (EMT) process. Cotreatment with N-acetyl-L-cysteine inhibited sulforaphane-inhibited invasion and upregulation of E-cadherin and almost completely abolished the sulforaphane-induced expression of Vimentin. The effect of sulforaphane on the growth of hepatocellular carcinoma cells was confirmed by a xenograft tumor growth model. All our finding indicated that sulforaphane is a promising and safe strategy for treating hepatocellular carcinoma.</description><subject>Animals</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>Bladder cancer</subject><subject>Carcinoma, Hepatocellular - drug therapy</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Movement</subject><subject>Cell Shape - drug effects</subject><subject>Colorectal cancer</subject><subject>Development and progression</subject><subject>epithelial-mesenchymal transition</subject><subject>Epithelial-Mesenchymal Transition - drug effects</subject><subject>Female</subject><subject>G1 Phase Cell Cycle Checkpoints</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Growth models</subject><subject>Health aspects</subject><subject>Hep G2 Cells</subject><subject>hepatocellular carcinoma</subject><subject>Hepatoma</subject><subject>Humans</subject><subject>Inhibitory Concentration 50</subject><subject>Isothiocyanates - pharmacology</subject><subject>Leukemia</subject><subject>Liver cancer</subject><subject>Liver Neoplasms - drug therapy</subject><subject>Liver Neoplasms - pathology</subject><subject>Medical prognosis</subject><subject>Metastasis</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Microscopy</subject><subject>Morphology</subject><subject>Neoplasm Invasiveness</subject><subject>Properties</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Studies</subject><subject>sulforaphane</subject><subject>Thiocyanates</subject><subject>Thyroid cancer</subject><subject>Transforming Growth Factor beta - physiology</subject><subject>Transforming growth factors</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkt9qFTEQxhdRbK3eeS0BwStz3PzZzeayFFuFghdW8G6Zk510U7LJmuxWz6v4GD6Iz2QOrbUFycWE4TffMDNfVb1k9UZ0mr-LacNr1m5kK7pH1SFTmlEuBXtc_jVnVIjm60H1LOeruuaqbvXT6oC3WjS6U4fVz8-rtzHBPEJA4sLotm7J5OLslP7-RV0YVoMDwdktI3oHnk6YMZhxN4EnS4KQ3eJiINGSEWdYokHvVw-JGEjGhTgB2acyuXZAighJCGZx10jij90lBpJnNA4zHXDGMGBYSJEZv8PuefXEgs_44jYeVV9O31-cfKDnn84-nhyfUyO7dqEcUMgtWGtbKRBtp5WpAUTdCGkVbMuOtq0CO1jNJLeMWd41Gk1rpSpRi6Pq9Y3unOK3FfPSX8U1hdKyZ1rwtpNa3aMuwWPvgo1lejO5bPpj2bACcSULtfkPVd6AkzMxoHUl_6Dgzb2CEcEvY45-3S81PwTf3oAmxZwT2n5OboK061nd743Qx9TvjdDvjVDwV7dDrdsJhzv47-X_Nc4zhMENMd8xMVHR0LqhXCsl_gAdRL3v</recordid><startdate>20160501</startdate><enddate>20160501</enddate><creator>WU, JINSHENG</creator><creator>HAN, JINGLI</creator><creator>HOU, BENXIN</creator><creator>DENG, CHENGWEI</creator><creator>WU, HUANLIANG</creator><creator>SHEN, LIANGFANG</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20160501</creationdate><title>Sulforaphane inhibits TGF-β-induced epithelial-mesenchymal transition of hepatocellular carcinoma cells via the reactive oxygen species-dependent pathway</title><author>WU, JINSHENG ; HAN, JINGLI ; HOU, BENXIN ; DENG, CHENGWEI ; WU, HUANLIANG ; SHEN, LIANGFANG</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c486t-2ae34bafff643eef897c0aa30534f7ab892b67afdf9142f11f2859ec6f4759e93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Antineoplastic Agents - 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metabolism</topic><topic>Studies</topic><topic>sulforaphane</topic><topic>Thiocyanates</topic><topic>Thyroid cancer</topic><topic>Transforming Growth Factor beta - physiology</topic><topic>Transforming growth factors</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>WU, JINSHENG</creatorcontrib><creatorcontrib>HAN, JINGLI</creatorcontrib><creatorcontrib>HOU, BENXIN</creatorcontrib><creatorcontrib>DENG, CHENGWEI</creatorcontrib><creatorcontrib>WU, HUANLIANG</creatorcontrib><creatorcontrib>SHEN, LIANGFANG</creatorcontrib><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>Medical Database (Alumni Edition)</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>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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 China</collection><jtitle>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>WU, JINSHENG</au><au>HAN, JINGLI</au><au>HOU, BENXIN</au><au>DENG, CHENGWEI</au><au>WU, HUANLIANG</au><au>SHEN, LIANGFANG</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sulforaphane inhibits TGF-β-induced epithelial-mesenchymal transition of hepatocellular carcinoma cells via the reactive oxygen species-dependent pathway</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2016-05-01</date><risdate>2016</risdate><volume>35</volume><issue>5</issue><spage>2977</spage><epage>2983</epage><pages>2977-2983</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>Sulforaphane is recognized as a safe antitumor agent derived from various cruciferous vegetables, including broccoli. It has been demonstrated that sulforaphase is a potent antitumor agent in diverse cancers. However, its effect on hepatocellular carcinoma remains largely unknown. Here, we show that sulforaphane inhibits TGF-β-induced epithelial-mesenchymal transition of hepatocellular carcinoma cell via the reactive oxygen species-dependent pathway. We found sulforaphane inhibited hepatocellular carcinoma cell proliferation in a dose- and time-dependent manner. Sulforaphane induced G0/G1 phase cell cycle arrest and promoted cell apoptosis. A set of experiments showed that sulforaphase inhibited hepatocellular carcinoma cell migration and invasion, inhibited the formation of fibroblast like mesenchymal cells and the expression of Vimentin, but increased the expression of E-cadherin, suggesting sulforaphane suppresses epithelial-mesenchymal transition (EMT) process. Cotreatment with N-acetyl-L-cysteine inhibited sulforaphane-inhibited invasion and upregulation of E-cadherin and almost completely abolished the sulforaphane-induced expression of Vimentin. The effect of sulforaphane on the growth of hepatocellular carcinoma cells was confirmed by a xenograft tumor growth model. All our finding indicated that sulforaphane is a promising and safe strategy for treating hepatocellular carcinoma.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>26935987</pmid><doi>10.3892/or.2016.4638</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Animals Antineoplastic Agents - pharmacology Apoptosis Bladder cancer Carcinoma, Hepatocellular - drug therapy Carcinoma, Hepatocellular - pathology Cell cycle Cell growth Cell Movement Cell Shape - drug effects Colorectal cancer Development and progression epithelial-mesenchymal transition Epithelial-Mesenchymal Transition - drug effects Female G1 Phase Cell Cycle Checkpoints Gene expression Genetic aspects Growth models Health aspects Hep G2 Cells hepatocellular carcinoma Hepatoma Humans Inhibitory Concentration 50 Isothiocyanates - pharmacology Leukemia Liver cancer Liver Neoplasms - drug therapy Liver Neoplasms - pathology Medical prognosis Metastasis Mice, Inbred BALB C Mice, Nude Microscopy Morphology Neoplasm Invasiveness Properties Reactive oxygen species Reactive Oxygen Species - metabolism Studies sulforaphane Thiocyanates Thyroid cancer Transforming Growth Factor beta - physiology Transforming growth factors Xenograft Model Antitumor Assays |
| title | Sulforaphane inhibits TGF-β-induced epithelial-mesenchymal transition of hepatocellular carcinoma cells via the reactive oxygen species-dependent pathway |
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