Clinical significance and function of RDH16 as a tumor‐suppressing gene in hepatocellular carcinoma
Aim Our previous transcriptome sequencing analysis detected that retinol dehydrogenase 16 (RDH16) was dramatically downregulated in hepatocellular carcinoma (HCC). RDH16 belongs to the short‐chain dehydrogenases/reductases super family, and its role in HCC remains unknown. This study aimed to invest...
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| Veröffentlicht in: | Hepatology research 2020-01, Vol.50 (1), p.110-120 |
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| creator | Zhu, Ying‐Hui Li, Jian‐Biao Wu, Rui‐Yan Yu, Yan Li, Xuan Li, Zhi‐Ling Zhang, Hai‐Liang Feng, Gong‐Kan Deng, Rong Zhu, Xiao‐Feng |
| description | Aim
Our previous transcriptome sequencing analysis detected that retinol dehydrogenase 16 (RDH16) was dramatically downregulated in hepatocellular carcinoma (HCC). RDH16 belongs to the short‐chain dehydrogenases/reductases super family, and its role in HCC remains unknown. This study aimed to investigate the expression and function of RDH16 in HCC.
Methods
The mRNA and protein level of RDH16 in HCC samples were detected by quantitative real‐time polymerase chain reaction and immunohistochemistry analyses, respectively. The role of RDH16 in HCC was determined by in vitro and in vivo functional studies.
Results
Downregulation of RDH16 has been detected in approximately 90% of primary HCCs, which was significantly associated with high serum alpha‐fetoprotein level, tumor size, microsatellite formation, thrombus, and poor overall survival of HCC patients. Compared with non‐tumor tissues, higher density of methylation was identified in HCC samples. In addition, RDH16 increases the level of retinoic acid and blocks the de novo synthesis of fatty acid in HCC cells. Functional study shows that ectopic expression of RDH16 in HCC cells suppresses cell growth, clonogenicity, and cell motility.
Conclusions
RDH16 might be a prognostic biomarker and intervention point for new therapeutic strategies in HCC. |
| doi_str_mv | 10.1111/hepr.13432 |
| format | Article |
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Our previous transcriptome sequencing analysis detected that retinol dehydrogenase 16 (RDH16) was dramatically downregulated in hepatocellular carcinoma (HCC). RDH16 belongs to the short‐chain dehydrogenases/reductases super family, and its role in HCC remains unknown. This study aimed to investigate the expression and function of RDH16 in HCC.
Methods
The mRNA and protein level of RDH16 in HCC samples were detected by quantitative real‐time polymerase chain reaction and immunohistochemistry analyses, respectively. The role of RDH16 in HCC was determined by in vitro and in vivo functional studies.
Results
Downregulation of RDH16 has been detected in approximately 90% of primary HCCs, which was significantly associated with high serum alpha‐fetoprotein level, tumor size, microsatellite formation, thrombus, and poor overall survival of HCC patients. Compared with non‐tumor tissues, higher density of methylation was identified in HCC samples. In addition, RDH16 increases the level of retinoic acid and blocks the de novo synthesis of fatty acid in HCC cells. Functional study shows that ectopic expression of RDH16 in HCC cells suppresses cell growth, clonogenicity, and cell motility.
Conclusions
RDH16 might be a prognostic biomarker and intervention point for new therapeutic strategies in HCC.</description><identifier>ISSN: 1386-6346</identifier><identifier>EISSN: 1872-034X</identifier><identifier>DOI: 10.1111/hepr.13432</identifier><identifier>PMID: 31661588</identifier><language>eng</language><publisher>Netherlands: Wiley Subscription Services, Inc</publisher><subject>Clinical significance ; Ectopic expression ; Gene expression ; Hepatocellular carcinoma ; Immunohistochemistry ; Liver cancer ; metastasis ; Polymerase chain reaction ; proliferation ; Retinoic acid ; Retinol dehydrogenase ; retinol dehydrogenase 16 ; Sequence analysis ; Thrombosis ; Vitamin A</subject><ispartof>Hepatology research, 2020-01, Vol.50 (1), p.110-120</ispartof><rights>2019 The Japan Society of Hepatology</rights><rights>2019 The Japan Society of Hepatology.</rights><rights>2020 The Japan Society of Hepatology</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3812-391e0ae56b3ce3891b74a276ab1336bf8ea4dfd6019dc26a026618a726fa92f03</citedby><cites>FETCH-LOGICAL-c3812-391e0ae56b3ce3891b74a276ab1336bf8ea4dfd6019dc26a026618a726fa92f03</cites><orcidid>0000-0003-3403-6645</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fhepr.13432$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fhepr.13432$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27923,27924,45573,45574</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31661588$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhu, Ying‐Hui</creatorcontrib><creatorcontrib>Li, Jian‐Biao</creatorcontrib><creatorcontrib>Wu, Rui‐Yan</creatorcontrib><creatorcontrib>Yu, Yan</creatorcontrib><creatorcontrib>Li, Xuan</creatorcontrib><creatorcontrib>Li, Zhi‐Ling</creatorcontrib><creatorcontrib>Zhang, Hai‐Liang</creatorcontrib><creatorcontrib>Feng, Gong‐Kan</creatorcontrib><creatorcontrib>Deng, Rong</creatorcontrib><creatorcontrib>Zhu, Xiao‐Feng</creatorcontrib><title>Clinical significance and function of RDH16 as a tumor‐suppressing gene in hepatocellular carcinoma</title><title>Hepatology research</title><addtitle>Hepatol Res</addtitle><description>Aim
Our previous transcriptome sequencing analysis detected that retinol dehydrogenase 16 (RDH16) was dramatically downregulated in hepatocellular carcinoma (HCC). RDH16 belongs to the short‐chain dehydrogenases/reductases super family, and its role in HCC remains unknown. This study aimed to investigate the expression and function of RDH16 in HCC.
Methods
The mRNA and protein level of RDH16 in HCC samples were detected by quantitative real‐time polymerase chain reaction and immunohistochemistry analyses, respectively. The role of RDH16 in HCC was determined by in vitro and in vivo functional studies.
Results
Downregulation of RDH16 has been detected in approximately 90% of primary HCCs, which was significantly associated with high serum alpha‐fetoprotein level, tumor size, microsatellite formation, thrombus, and poor overall survival of HCC patients. Compared with non‐tumor tissues, higher density of methylation was identified in HCC samples. In addition, RDH16 increases the level of retinoic acid and blocks the de novo synthesis of fatty acid in HCC cells. Functional study shows that ectopic expression of RDH16 in HCC cells suppresses cell growth, clonogenicity, and cell motility.
Conclusions
RDH16 might be a prognostic biomarker and intervention point for new therapeutic strategies in HCC.</description><subject>Clinical significance</subject><subject>Ectopic expression</subject><subject>Gene expression</subject><subject>Hepatocellular carcinoma</subject><subject>Immunohistochemistry</subject><subject>Liver cancer</subject><subject>metastasis</subject><subject>Polymerase chain reaction</subject><subject>proliferation</subject><subject>Retinoic acid</subject><subject>Retinol dehydrogenase</subject><subject>retinol dehydrogenase 16</subject><subject>Sequence analysis</subject><subject>Thrombosis</subject><subject>Vitamin A</subject><issn>1386-6346</issn><issn>1872-034X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNp9kM9qFEEQhxsxmBi9-ADS4EWEif1ntqbnKJvoCgElKHgbanqq1w4z3WP3DpKbj5BnzJPY68YcPFiXqsPHj199jL2Q4kyWefud5nQmda3VI3YiTaMqoetvj8utDVSgazhmT3O-FkI2QtVP2LGWAHJlzAmj9eiDtzjy7LfBu3IGSxzDwN0S7M7HwKPjV-cbCRwzR75bppjuft3mZZ4T5ezDlm8pEPeBlya4i5bGcRkxcYvJ-hAnfMaOHI6Znt_vU_b1_cWX9aa6_PTh4_rdZWW1karSrSSBtIJeW9KmlX1To2oAe6k19M4Q1oMbQMh2sApQqPKGwUaBw1Y5oU_Z60PunOKPhfKum3ze18FAccmd0lIAGGihoK_-Qa_jkkJpV6ha10qvQBfqzYGyKeacyHVz8hOmm06Kbi-_28vv_sgv8Mv7yKWfaHhA_9ougDwAP_1IN_-J6jYXn68Oob8BT62Png</recordid><startdate>202001</startdate><enddate>202001</enddate><creator>Zhu, Ying‐Hui</creator><creator>Li, Jian‐Biao</creator><creator>Wu, Rui‐Yan</creator><creator>Yu, Yan</creator><creator>Li, Xuan</creator><creator>Li, Zhi‐Ling</creator><creator>Zhang, Hai‐Liang</creator><creator>Feng, Gong‐Kan</creator><creator>Deng, Rong</creator><creator>Zhu, Xiao‐Feng</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7TM</scope><scope>7U9</scope><scope>H94</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-3403-6645</orcidid></search><sort><creationdate>202001</creationdate><title>Clinical significance and function of RDH16 as a tumor‐suppressing gene in hepatocellular carcinoma</title><author>Zhu, Ying‐Hui ; Li, Jian‐Biao ; Wu, Rui‐Yan ; Yu, Yan ; Li, Xuan ; Li, Zhi‐Ling ; Zhang, Hai‐Liang ; Feng, Gong‐Kan ; Deng, Rong ; Zhu, Xiao‐Feng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3812-391e0ae56b3ce3891b74a276ab1336bf8ea4dfd6019dc26a026618a726fa92f03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Clinical significance</topic><topic>Ectopic expression</topic><topic>Gene expression</topic><topic>Hepatocellular carcinoma</topic><topic>Immunohistochemistry</topic><topic>Liver cancer</topic><topic>metastasis</topic><topic>Polymerase chain reaction</topic><topic>proliferation</topic><topic>Retinoic acid</topic><topic>Retinol dehydrogenase</topic><topic>retinol dehydrogenase 16</topic><topic>Sequence analysis</topic><topic>Thrombosis</topic><topic>Vitamin A</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhu, Ying‐Hui</creatorcontrib><creatorcontrib>Li, Jian‐Biao</creatorcontrib><creatorcontrib>Wu, Rui‐Yan</creatorcontrib><creatorcontrib>Yu, Yan</creatorcontrib><creatorcontrib>Li, Xuan</creatorcontrib><creatorcontrib>Li, Zhi‐Ling</creatorcontrib><creatorcontrib>Zhang, Hai‐Liang</creatorcontrib><creatorcontrib>Feng, Gong‐Kan</creatorcontrib><creatorcontrib>Deng, Rong</creatorcontrib><creatorcontrib>Zhu, Xiao‐Feng</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Hepatology research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhu, Ying‐Hui</au><au>Li, Jian‐Biao</au><au>Wu, Rui‐Yan</au><au>Yu, Yan</au><au>Li, Xuan</au><au>Li, Zhi‐Ling</au><au>Zhang, Hai‐Liang</au><au>Feng, Gong‐Kan</au><au>Deng, Rong</au><au>Zhu, Xiao‐Feng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Clinical significance and function of RDH16 as a tumor‐suppressing gene in hepatocellular carcinoma</atitle><jtitle>Hepatology research</jtitle><addtitle>Hepatol Res</addtitle><date>2020-01</date><risdate>2020</risdate><volume>50</volume><issue>1</issue><spage>110</spage><epage>120</epage><pages>110-120</pages><issn>1386-6346</issn><eissn>1872-034X</eissn><abstract>Aim
Our previous transcriptome sequencing analysis detected that retinol dehydrogenase 16 (RDH16) was dramatically downregulated in hepatocellular carcinoma (HCC). RDH16 belongs to the short‐chain dehydrogenases/reductases super family, and its role in HCC remains unknown. This study aimed to investigate the expression and function of RDH16 in HCC.
Methods
The mRNA and protein level of RDH16 in HCC samples were detected by quantitative real‐time polymerase chain reaction and immunohistochemistry analyses, respectively. The role of RDH16 in HCC was determined by in vitro and in vivo functional studies.
Results
Downregulation of RDH16 has been detected in approximately 90% of primary HCCs, which was significantly associated with high serum alpha‐fetoprotein level, tumor size, microsatellite formation, thrombus, and poor overall survival of HCC patients. Compared with non‐tumor tissues, higher density of methylation was identified in HCC samples. In addition, RDH16 increases the level of retinoic acid and blocks the de novo synthesis of fatty acid in HCC cells. Functional study shows that ectopic expression of RDH16 in HCC cells suppresses cell growth, clonogenicity, and cell motility.
Conclusions
RDH16 might be a prognostic biomarker and intervention point for new therapeutic strategies in HCC.</abstract><cop>Netherlands</cop><pub>Wiley Subscription Services, Inc</pub><pmid>31661588</pmid><doi>10.1111/hepr.13432</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0003-3403-6645</orcidid></addata></record> |
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| source | Wiley Online Library All Journals |
| subjects | Clinical significance Ectopic expression Gene expression Hepatocellular carcinoma Immunohistochemistry Liver cancer metastasis Polymerase chain reaction proliferation Retinoic acid Retinol dehydrogenase retinol dehydrogenase 16 Sequence analysis Thrombosis Vitamin A |
| title | Clinical significance and function of RDH16 as a tumor‐suppressing gene in hepatocellular carcinoma |
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