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lncRNA‐POIR promotes epithelial–mesenchymal transition and suppresses sorafenib sensitivity simultaneously in hepatocellular carcinoma by sponging miR‐182‐5p
Sorafenib (SOR) resistance remains a major obstacle in the effective treatment of hepatocellular carcinoma (HCC). A number of long noncoding RNAs (lncRNAs) are responsible for this chemoresistance. This study aimed to reveal the essential function of a recently defined lncRNA, lncRNA‐POIR, in the ep...
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| Published in: | Journal of cellular biochemistry 2021-01, Vol.122 (1), p.130-142 |
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| container_title | Journal of cellular biochemistry |
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| creator | Chen, Bryan Wei Zhou, Yue Wei, Tao Wen, Liang Zhang, Yi‐bo Shen, Shi‐chao Zhang, Jian Ma, Tao Chen, Wen Ni, Lei Wang, Yi Bai, Xue‐li Liang, Ting‐bo |
| description | Sorafenib (SOR) resistance remains a major obstacle in the effective treatment of hepatocellular carcinoma (HCC). A number of long noncoding RNAs (lncRNAs) are responsible for this chemoresistance. This study aimed to reveal the essential function of a recently defined lncRNA, lncRNA‐POIR, in the epithelial–mesenchymal transition (EMT) and SOR sensitivity of HCC cells. SOR‐induced cytotoxicity was analyzed via cell counting kit‐8 and ethynyl‐2'‐deoxyuridine incorporation assays, whereas immunoblotting and confocal immunofluorescence were used to determine the expression levels of EMT markers. Furthermore, loss‐ or gain‐of‐function approaches were used to demonstrate the role of lncRNA‐POIR/miR‐182‐5p on EMT and SOR sensitivity in HCC. The direct interaction between lncRNA‐POIR and miR‐182‐5p was verified using a luciferase reporter assay. We found that knockdown of lncRNA‐POIR sensitized HCC cells to SOR and simultaneously reversed EMT. As expected, miR‐182‐5p was confirmed as the downstream target of lncRNA‐POIR. Moreover, miR‐182‐5p overexpression clearly reversed EMT and promoted SOR‐induced cytotoxicity in representative HCC cells, whereas miR‐182‐5p downregulation played a contrasting role; miR‐182‐5p knockdown abolished the modulatory effects of lncRNA‐POIR siRNA on EMT and SOR sensitivity. Together, these pieces of data suggest that lncRNA‐POIR promotes EMT progression and suppresses SOR sensitivity simultaneously by sponging miR‐182‐5p. Thus, we proposed a compelling rationale for the use of lncRNA‐POIR as a promising predictor of SOR response and as a potential therapeutic target for HCC treatment in the future.
In this study, we verified the biological functions of lncRNA‐POIR as an aberrantly expressed lncRNA in hepatocellular carcinoma (HCC) cells. lncRNA‐POIR modulated EMT and sorafenib sensitivity of HCC cells via functioning as a competing endogenous RNA (ceRNA) of miR‐182‐5p. Our findings provide a compelling rationale for the use of lncRNA‐POIR as a predictor of SOR response and a promising therapeutic target for future HCC treatment. |
| doi_str_mv | 10.1002/jcb.29844 |
| format | article |
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In this study, we verified the biological functions of lncRNA‐POIR as an aberrantly expressed lncRNA in hepatocellular carcinoma (HCC) cells. lncRNA‐POIR modulated EMT and sorafenib sensitivity of HCC cells via functioning as a competing endogenous RNA (ceRNA) of miR‐182‐5p. Our findings provide a compelling rationale for the use of lncRNA‐POIR as a predictor of SOR response and a promising therapeutic target for future HCC treatment.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/jcb.29844</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc</publisher><subject>Chemoresistance ; Cytotoxicity ; epithelial–mesenchymal transition ; Hepatocellular carcinoma ; Immunoblotting ; Immunofluorescence ; Liver cancer ; lncRNA‐POIR ; Mesenchyme ; miR‐182‐5p ; siRNA ; sorafenib sensitivity ; Targeted cancer therapy ; Toxicity</subject><ispartof>Journal of cellular biochemistry, 2021-01, Vol.122 (1), p.130-142</ispartof><rights>2020 Wiley Periodicals LLC</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3304-e6d84622ea97e36a2c8b1605ddab19ace1577dd3cdaa1da1d553a2571723e72b3</citedby><cites>FETCH-LOGICAL-c3304-e6d84622ea97e36a2c8b1605ddab19ace1577dd3cdaa1da1d553a2571723e72b3</cites><orcidid>0000-0001-7385-1867</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcb.29844$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcb.29844$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,786,790,27957,27958,50923,51032</link.rule.ids></links><search><creatorcontrib>Chen, Bryan Wei</creatorcontrib><creatorcontrib>Zhou, Yue</creatorcontrib><creatorcontrib>Wei, Tao</creatorcontrib><creatorcontrib>Wen, Liang</creatorcontrib><creatorcontrib>Zhang, Yi‐bo</creatorcontrib><creatorcontrib>Shen, Shi‐chao</creatorcontrib><creatorcontrib>Zhang, Jian</creatorcontrib><creatorcontrib>Ma, Tao</creatorcontrib><creatorcontrib>Chen, Wen</creatorcontrib><creatorcontrib>Ni, Lei</creatorcontrib><creatorcontrib>Wang, Yi</creatorcontrib><creatorcontrib>Bai, Xue‐li</creatorcontrib><creatorcontrib>Liang, Ting‐bo</creatorcontrib><title>lncRNA‐POIR promotes epithelial–mesenchymal transition and suppresses sorafenib sensitivity simultaneously in hepatocellular carcinoma by sponging miR‐182‐5p</title><title>Journal of cellular biochemistry</title><description>Sorafenib (SOR) resistance remains a major obstacle in the effective treatment of hepatocellular carcinoma (HCC). A number of long noncoding RNAs (lncRNAs) are responsible for this chemoresistance. This study aimed to reveal the essential function of a recently defined lncRNA, lncRNA‐POIR, in the epithelial–mesenchymal transition (EMT) and SOR sensitivity of HCC cells. SOR‐induced cytotoxicity was analyzed via cell counting kit‐8 and ethynyl‐2'‐deoxyuridine incorporation assays, whereas immunoblotting and confocal immunofluorescence were used to determine the expression levels of EMT markers. Furthermore, loss‐ or gain‐of‐function approaches were used to demonstrate the role of lncRNA‐POIR/miR‐182‐5p on EMT and SOR sensitivity in HCC. The direct interaction between lncRNA‐POIR and miR‐182‐5p was verified using a luciferase reporter assay. We found that knockdown of lncRNA‐POIR sensitized HCC cells to SOR and simultaneously reversed EMT. As expected, miR‐182‐5p was confirmed as the downstream target of lncRNA‐POIR. Moreover, miR‐182‐5p overexpression clearly reversed EMT and promoted SOR‐induced cytotoxicity in representative HCC cells, whereas miR‐182‐5p downregulation played a contrasting role; miR‐182‐5p knockdown abolished the modulatory effects of lncRNA‐POIR siRNA on EMT and SOR sensitivity. Together, these pieces of data suggest that lncRNA‐POIR promotes EMT progression and suppresses SOR sensitivity simultaneously by sponging miR‐182‐5p. Thus, we proposed a compelling rationale for the use of lncRNA‐POIR as a promising predictor of SOR response and as a potential therapeutic target for HCC treatment in the future.
In this study, we verified the biological functions of lncRNA‐POIR as an aberrantly expressed lncRNA in hepatocellular carcinoma (HCC) cells. lncRNA‐POIR modulated EMT and sorafenib sensitivity of HCC cells via functioning as a competing endogenous RNA (ceRNA) of miR‐182‐5p. Our findings provide a compelling rationale for the use of lncRNA‐POIR as a predictor of SOR response and a promising therapeutic target for future HCC treatment.</description><subject>Chemoresistance</subject><subject>Cytotoxicity</subject><subject>epithelial–mesenchymal transition</subject><subject>Hepatocellular carcinoma</subject><subject>Immunoblotting</subject><subject>Immunofluorescence</subject><subject>Liver cancer</subject><subject>lncRNA‐POIR</subject><subject>Mesenchyme</subject><subject>miR‐182‐5p</subject><subject>siRNA</subject><subject>sorafenib sensitivity</subject><subject>Targeted cancer therapy</subject><subject>Toxicity</subject><issn>0730-2312</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNp10ctu1DAUBmALUYmhZcEbWGIDi7S-JZ4sy4hLUUWrEayjE-dMxyPHDnYCyq6PgMQz8GJ9EjyEFVIly958x_p1fkJecnbOGRMXB9Oei3qt1BOy4qzWhaqUekpWTEtWCMnFM_I8pQNjrK6lWJHfzpvt58uH-5-3N1dbOsTQhxETxcGOe3QW3MP9rx4TerOfe3B0jOCTHW3wFHxH0zQMEVPKIylE2KG3Lc36SL7bcabJ9pMbwWOYkpup9XSPA4zBoHOTg0gNRGN96IG2WQ_B31l_R3u7zZn4WuS7HM7IyQ5cwhf_3lPy9f27L5uPxfXNh6vN5XVhpGSqwKpbq0oIhFqjrECYdcsrVnYdtLwGg7zUuuuk6QB4l09ZShCl5lpI1KKVp-T18m_ew7cJ09j0Nh2TLvkboZSqmBRVnemr_-ghTNHndFlVpdJS1DKrN4syMaQUcdcM0fYQ54az5lhYkwtr_haW7cVif1iH8-Ow-bR5u0z8ASgsnzI</recordid><startdate>202101</startdate><enddate>202101</enddate><creator>Chen, Bryan Wei</creator><creator>Zhou, Yue</creator><creator>Wei, Tao</creator><creator>Wen, Liang</creator><creator>Zhang, Yi‐bo</creator><creator>Shen, Shi‐chao</creator><creator>Zhang, Jian</creator><creator>Ma, Tao</creator><creator>Chen, Wen</creator><creator>Ni, Lei</creator><creator>Wang, Yi</creator><creator>Bai, Xue‐li</creator><creator>Liang, Ting‐bo</creator><general>Wiley Subscription Services, Inc</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-7385-1867</orcidid></search><sort><creationdate>202101</creationdate><title>lncRNA‐POIR promotes epithelial–mesenchymal transition and suppresses sorafenib sensitivity simultaneously in hepatocellular carcinoma by sponging miR‐182‐5p</title><author>Chen, Bryan Wei ; Zhou, Yue ; Wei, Tao ; Wen, Liang ; Zhang, Yi‐bo ; Shen, Shi‐chao ; Zhang, Jian ; Ma, Tao ; Chen, Wen ; Ni, Lei ; Wang, Yi ; Bai, Xue‐li ; Liang, Ting‐bo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3304-e6d84622ea97e36a2c8b1605ddab19ace1577dd3cdaa1da1d553a2571723e72b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Chemoresistance</topic><topic>Cytotoxicity</topic><topic>epithelial–mesenchymal transition</topic><topic>Hepatocellular carcinoma</topic><topic>Immunoblotting</topic><topic>Immunofluorescence</topic><topic>Liver cancer</topic><topic>lncRNA‐POIR</topic><topic>Mesenchyme</topic><topic>miR‐182‐5p</topic><topic>siRNA</topic><topic>sorafenib sensitivity</topic><topic>Targeted cancer therapy</topic><topic>Toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Bryan Wei</creatorcontrib><creatorcontrib>Zhou, Yue</creatorcontrib><creatorcontrib>Wei, Tao</creatorcontrib><creatorcontrib>Wen, Liang</creatorcontrib><creatorcontrib>Zhang, Yi‐bo</creatorcontrib><creatorcontrib>Shen, Shi‐chao</creatorcontrib><creatorcontrib>Zhang, Jian</creatorcontrib><creatorcontrib>Ma, Tao</creatorcontrib><creatorcontrib>Chen, Wen</creatorcontrib><creatorcontrib>Ni, Lei</creatorcontrib><creatorcontrib>Wang, Yi</creatorcontrib><creatorcontrib>Bai, Xue‐li</creatorcontrib><creatorcontrib>Liang, Ting‐bo</creatorcontrib><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Bryan Wei</au><au>Zhou, Yue</au><au>Wei, Tao</au><au>Wen, Liang</au><au>Zhang, Yi‐bo</au><au>Shen, Shi‐chao</au><au>Zhang, Jian</au><au>Ma, Tao</au><au>Chen, Wen</au><au>Ni, Lei</au><au>Wang, Yi</au><au>Bai, Xue‐li</au><au>Liang, Ting‐bo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>lncRNA‐POIR promotes epithelial–mesenchymal transition and suppresses sorafenib sensitivity simultaneously in hepatocellular carcinoma by sponging miR‐182‐5p</atitle><jtitle>Journal of cellular biochemistry</jtitle><date>2021-01</date><risdate>2021</risdate><volume>122</volume><issue>1</issue><spage>130</spage><epage>142</epage><pages>130-142</pages><issn>0730-2312</issn><eissn>1097-4644</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Sorafenib (SOR) resistance remains a major obstacle in the effective treatment of hepatocellular carcinoma (HCC). A number of long noncoding RNAs (lncRNAs) are responsible for this chemoresistance. This study aimed to reveal the essential function of a recently defined lncRNA, lncRNA‐POIR, in the epithelial–mesenchymal transition (EMT) and SOR sensitivity of HCC cells. SOR‐induced cytotoxicity was analyzed via cell counting kit‐8 and ethynyl‐2'‐deoxyuridine incorporation assays, whereas immunoblotting and confocal immunofluorescence were used to determine the expression levels of EMT markers. Furthermore, loss‐ or gain‐of‐function approaches were used to demonstrate the role of lncRNA‐POIR/miR‐182‐5p on EMT and SOR sensitivity in HCC. The direct interaction between lncRNA‐POIR and miR‐182‐5p was verified using a luciferase reporter assay. We found that knockdown of lncRNA‐POIR sensitized HCC cells to SOR and simultaneously reversed EMT. As expected, miR‐182‐5p was confirmed as the downstream target of lncRNA‐POIR. Moreover, miR‐182‐5p overexpression clearly reversed EMT and promoted SOR‐induced cytotoxicity in representative HCC cells, whereas miR‐182‐5p downregulation played a contrasting role; miR‐182‐5p knockdown abolished the modulatory effects of lncRNA‐POIR siRNA on EMT and SOR sensitivity. Together, these pieces of data suggest that lncRNA‐POIR promotes EMT progression and suppresses SOR sensitivity simultaneously by sponging miR‐182‐5p. Thus, we proposed a compelling rationale for the use of lncRNA‐POIR as a promising predictor of SOR response and as a potential therapeutic target for HCC treatment in the future.
In this study, we verified the biological functions of lncRNA‐POIR as an aberrantly expressed lncRNA in hepatocellular carcinoma (HCC) cells. lncRNA‐POIR modulated EMT and sorafenib sensitivity of HCC cells via functioning as a competing endogenous RNA (ceRNA) of miR‐182‐5p. Our findings provide a compelling rationale for the use of lncRNA‐POIR as a predictor of SOR response and a promising therapeutic target for future HCC treatment.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc</pub><doi>10.1002/jcb.29844</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0001-7385-1867</orcidid></addata></record> |
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| subjects | Chemoresistance Cytotoxicity epithelial–mesenchymal transition Hepatocellular carcinoma Immunoblotting Immunofluorescence Liver cancer lncRNA‐POIR Mesenchyme miR‐182‐5p siRNA sorafenib sensitivity Targeted cancer therapy Toxicity |
| title | lncRNA‐POIR promotes epithelial–mesenchymal transition and suppresses sorafenib sensitivity simultaneously in hepatocellular carcinoma by sponging miR‐182‐5p |
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