miR-424-5p represses the metastasis and invasion of intrahepatic cholangiocarcinoma by targeting ARK5
MicroRNAs (miRNAs) have been validated to play prominent roles in the occurrence and development of many kinds of malignant cancer. MiR-424-5p has been reported to participate in various tumors proliferation and metastasis as a suppressor. On the contrary, miR-424-5p would promote cell proliferation...
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| Veröffentlicht in: | International journal of biological sciences 2019-01, Vol.15 (8), p.1591-1599 |
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| container_title | International journal of biological sciences |
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| creator | Wu, Jingbang Yang, Beng Zhang, Yanpeng Feng, Xiaode He, Bin Xie, Haiyang Zhou, Lin Wu, Jian Zheng, Shusen |
| description | MicroRNAs (miRNAs) have been validated to play prominent roles in the occurrence and development of many kinds of malignant cancer. MiR-424-5p has been reported to participate in various tumors proliferation and metastasis as a suppressor. On the contrary, miR-424-5p would promote cell proliferation in some tumors. However, the expression of miR-424-5p in intrahepatic cholangiocarcinoma (ICC) is rarely reported and its mechanism remains unclear. Here, we discover that miR-424-5p is frequently downregulated in ICC tissues compared with adjacent normal tissues and in ICC cells. Over-expression of miR-424-5p significantly inhibits the invasion and migration of ICC cells
. Importantly, miR-424-5p is found to be a suppressor of ARK5, by binding to 3'-UTR of ARK5 mRNA and then inhibiting mTOR phosphorylated, thus deregulating epithelial-mesenchymal transition (EMT) of ICC. Furthermore, ARK5 is found to play a role in ICC metastasis and regulating EMT. Knockdown of ARK5 inhibits invasion and migration of ICC, while the over-expression gives an opposite effect. Besides, high-expression of ARK5 is also associated with poor prognosis. In conclusion, our study reveals that miR-424-5p is critical to the invasion, migration and EMT progression in ICC cells. Targeting the pathway described here may be a novel approach to inhibit metastasis of ICC and the restoration of miR-424-5p expression may be a promising strategy for ICC therapy. |
| doi_str_mv | 10.7150/ijbs.34113 |
| format | Article |
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. Importantly, miR-424-5p is found to be a suppressor of ARK5, by binding to 3'-UTR of ARK5 mRNA and then inhibiting mTOR phosphorylated, thus deregulating epithelial-mesenchymal transition (EMT) of ICC. Furthermore, ARK5 is found to play a role in ICC metastasis and regulating EMT. Knockdown of ARK5 inhibits invasion and migration of ICC, while the over-expression gives an opposite effect. Besides, high-expression of ARK5 is also associated with poor prognosis. In conclusion, our study reveals that miR-424-5p is critical to the invasion, migration and EMT progression in ICC cells. Targeting the pathway described here may be a novel approach to inhibit metastasis of ICC and the restoration of miR-424-5p expression may be a promising strategy for ICC therapy.</description><identifier>ISSN: 1449-2288</identifier><identifier>EISSN: 1449-2288</identifier><identifier>DOI: 10.7150/ijbs.34113</identifier><identifier>PMID: 31360102</identifier><language>eng</language><publisher>Australia: Ivyspring International Publisher Pty Ltd</publisher><subject>3' Untranslated regions ; Blotting, Western ; Cell Line ; Cell Line, Tumor ; Cell migration ; Cell Movement - genetics ; Cell Movement - physiology ; Cell proliferation ; Cell Proliferation - genetics ; Cell Proliferation - physiology ; Cell Survival - genetics ; Cell Survival - physiology ; Cholangiocarcinoma ; Cholangiocarcinoma - genetics ; Cholangiocarcinoma - metabolism ; Deregulation ; Gene Expression Regulation, Neoplastic - genetics ; Humans ; Liver Neoplasms - genetics ; Liver Neoplasms - metabolism ; Mesenchyme ; Metastases ; Metastasis ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; mRNA ; Overexpression ; Protein Kinases - genetics ; Protein Kinases - metabolism ; Repressor Proteins - genetics ; Repressor Proteins - metabolism ; Research Paper ; Restoration ; TOR protein ; Tumors</subject><ispartof>International journal of biological sciences, 2019-01, Vol.15 (8), p.1591-1599</ispartof><rights>Copyright BioMed Central 2019</rights><rights>Ivyspring International Publisher 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c406t-6aaef7513a5088613a8629e5419c8741c64b76765aceb80e816f770bd09b0e6e3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6643209/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6643209/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31360102$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Jingbang</creatorcontrib><creatorcontrib>Yang, Beng</creatorcontrib><creatorcontrib>Zhang, Yanpeng</creatorcontrib><creatorcontrib>Feng, Xiaode</creatorcontrib><creatorcontrib>He, Bin</creatorcontrib><creatorcontrib>Xie, Haiyang</creatorcontrib><creatorcontrib>Zhou, Lin</creatorcontrib><creatorcontrib>Wu, Jian</creatorcontrib><creatorcontrib>Zheng, Shusen</creatorcontrib><title>miR-424-5p represses the metastasis and invasion of intrahepatic cholangiocarcinoma by targeting ARK5</title><title>International journal of biological sciences</title><addtitle>Int J Biol Sci</addtitle><description>MicroRNAs (miRNAs) have been validated to play prominent roles in the occurrence and development of many kinds of malignant cancer. MiR-424-5p has been reported to participate in various tumors proliferation and metastasis as a suppressor. On the contrary, miR-424-5p would promote cell proliferation in some tumors. However, the expression of miR-424-5p in intrahepatic cholangiocarcinoma (ICC) is rarely reported and its mechanism remains unclear. Here, we discover that miR-424-5p is frequently downregulated in ICC tissues compared with adjacent normal tissues and in ICC cells. Over-expression of miR-424-5p significantly inhibits the invasion and migration of ICC cells
. Importantly, miR-424-5p is found to be a suppressor of ARK5, by binding to 3'-UTR of ARK5 mRNA and then inhibiting mTOR phosphorylated, thus deregulating epithelial-mesenchymal transition (EMT) of ICC. Furthermore, ARK5 is found to play a role in ICC metastasis and regulating EMT. Knockdown of ARK5 inhibits invasion and migration of ICC, while the over-expression gives an opposite effect. Besides, high-expression of ARK5 is also associated with poor prognosis. In conclusion, our study reveals that miR-424-5p is critical to the invasion, migration and EMT progression in ICC cells. Targeting the pathway described here may be a novel approach to inhibit metastasis of ICC and the restoration of miR-424-5p expression may be a promising strategy for ICC therapy.</description><subject>3' Untranslated regions</subject><subject>Blotting, Western</subject><subject>Cell Line</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement - genetics</subject><subject>Cell Movement - physiology</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - genetics</subject><subject>Cell Proliferation - physiology</subject><subject>Cell Survival - genetics</subject><subject>Cell Survival - physiology</subject><subject>Cholangiocarcinoma</subject><subject>Cholangiocarcinoma - genetics</subject><subject>Cholangiocarcinoma - metabolism</subject><subject>Deregulation</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Humans</subject><subject>Liver Neoplasms - genetics</subject><subject>Liver Neoplasms - metabolism</subject><subject>Mesenchyme</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>mRNA</subject><subject>Overexpression</subject><subject>Protein Kinases - genetics</subject><subject>Protein Kinases - metabolism</subject><subject>Repressor Proteins - genetics</subject><subject>Repressor Proteins - metabolism</subject><subject>Research Paper</subject><subject>Restoration</subject><subject>TOR protein</subject><subject>Tumors</subject><issn>1449-2288</issn><issn>1449-2288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkVtLAzEQhYMo3l_8ARLwRYTVZHPdF6GINywIos8hm862Kd3NmmwF_72pVlFhYA7Mx-EMB6EjSs4VFeTCz-t0zjilbAPtUs6roiy13vyld9BeSnNCmBSabKMdRpkklJS7CFr_VPCSF6LHEfoIKUHCwwxwC4NNeXzCtptg371lHTocmqyHaGfQ28E77GZhYbupD85G57vQWly_48HGKQy-m-LR04M4QFuNXSQ4XO999HJz_Xx1V4wfb--vRuPCcSKHQloLjRKUWUG0lnlrWVYgOK2cVpw6yWsllRTWQa0JaCobpUg9IVVNQALbR5dfvv2ybmHiYBV0YfroWxvfTbDe_L10fmam4c1IyVlJqmxwujaI4XUJaTCtTw4W-UMIy2TKUipChaA8oyf_0HlYxi6_t6K0oJIqlamzL8rFkFKE5icMJWbVnlm1Zz7by_Dx7_g_6Hdd7AOta5W8</recordid><startdate>20190101</startdate><enddate>20190101</enddate><creator>Wu, Jingbang</creator><creator>Yang, Beng</creator><creator>Zhang, Yanpeng</creator><creator>Feng, Xiaode</creator><creator>He, Bin</creator><creator>Xie, Haiyang</creator><creator>Zhou, Lin</creator><creator>Wu, Jian</creator><creator>Zheng, Shusen</creator><general>Ivyspring International Publisher Pty Ltd</general><general>Ivyspring International Publisher</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>7QL</scope><scope>7QO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20190101</creationdate><title>miR-424-5p represses the metastasis and invasion of intrahepatic cholangiocarcinoma by targeting ARK5</title><author>Wu, Jingbang ; Yang, Beng ; Zhang, Yanpeng ; Feng, Xiaode ; He, Bin ; Xie, Haiyang ; Zhou, Lin ; Wu, Jian ; Zheng, Shusen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c406t-6aaef7513a5088613a8629e5419c8741c64b76765aceb80e816f770bd09b0e6e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>3' Untranslated regions</topic><topic>Blotting, Western</topic><topic>Cell Line</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Movement - genetics</topic><topic>Cell Movement - physiology</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - genetics</topic><topic>Cell Proliferation - physiology</topic><topic>Cell Survival - genetics</topic><topic>Cell Survival - physiology</topic><topic>Cholangiocarcinoma</topic><topic>Cholangiocarcinoma - genetics</topic><topic>Cholangiocarcinoma - metabolism</topic><topic>Deregulation</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Humans</topic><topic>Liver Neoplasms - genetics</topic><topic>Liver Neoplasms - metabolism</topic><topic>Mesenchyme</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>mRNA</topic><topic>Overexpression</topic><topic>Protein Kinases - genetics</topic><topic>Protein Kinases - metabolism</topic><topic>Repressor Proteins - genetics</topic><topic>Repressor Proteins - metabolism</topic><topic>Research Paper</topic><topic>Restoration</topic><topic>TOR protein</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Jingbang</creatorcontrib><creatorcontrib>Yang, Beng</creatorcontrib><creatorcontrib>Zhang, Yanpeng</creatorcontrib><creatorcontrib>Feng, Xiaode</creatorcontrib><creatorcontrib>He, Bin</creatorcontrib><creatorcontrib>Xie, Haiyang</creatorcontrib><creatorcontrib>Zhou, Lin</creatorcontrib><creatorcontrib>Wu, Jian</creatorcontrib><creatorcontrib>Zheng, Shusen</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research 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>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of biological sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Jingbang</au><au>Yang, Beng</au><au>Zhang, Yanpeng</au><au>Feng, Xiaode</au><au>He, Bin</au><au>Xie, Haiyang</au><au>Zhou, Lin</au><au>Wu, Jian</au><au>Zheng, Shusen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR-424-5p represses the metastasis and invasion of intrahepatic cholangiocarcinoma by targeting ARK5</atitle><jtitle>International journal of biological sciences</jtitle><addtitle>Int J Biol Sci</addtitle><date>2019-01-01</date><risdate>2019</risdate><volume>15</volume><issue>8</issue><spage>1591</spage><epage>1599</epage><pages>1591-1599</pages><issn>1449-2288</issn><eissn>1449-2288</eissn><abstract>MicroRNAs (miRNAs) have been validated to play prominent roles in the occurrence and development of many kinds of malignant cancer. MiR-424-5p has been reported to participate in various tumors proliferation and metastasis as a suppressor. On the contrary, miR-424-5p would promote cell proliferation in some tumors. However, the expression of miR-424-5p in intrahepatic cholangiocarcinoma (ICC) is rarely reported and its mechanism remains unclear. Here, we discover that miR-424-5p is frequently downregulated in ICC tissues compared with adjacent normal tissues and in ICC cells. Over-expression of miR-424-5p significantly inhibits the invasion and migration of ICC cells
. Importantly, miR-424-5p is found to be a suppressor of ARK5, by binding to 3'-UTR of ARK5 mRNA and then inhibiting mTOR phosphorylated, thus deregulating epithelial-mesenchymal transition (EMT) of ICC. Furthermore, ARK5 is found to play a role in ICC metastasis and regulating EMT. Knockdown of ARK5 inhibits invasion and migration of ICC, while the over-expression gives an opposite effect. Besides, high-expression of ARK5 is also associated with poor prognosis. In conclusion, our study reveals that miR-424-5p is critical to the invasion, migration and EMT progression in ICC cells. Targeting the pathway described here may be a novel approach to inhibit metastasis of ICC and the restoration of miR-424-5p expression may be a promising strategy for ICC therapy.</abstract><cop>Australia</cop><pub>Ivyspring International Publisher Pty Ltd</pub><pmid>31360102</pmid><doi>10.7150/ijbs.34113</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 3' Untranslated regions Blotting, Western Cell Line Cell Line, Tumor Cell migration Cell Movement - genetics Cell Movement - physiology Cell proliferation Cell Proliferation - genetics Cell Proliferation - physiology Cell Survival - genetics Cell Survival - physiology Cholangiocarcinoma Cholangiocarcinoma - genetics Cholangiocarcinoma - metabolism Deregulation Gene Expression Regulation, Neoplastic - genetics Humans Liver Neoplasms - genetics Liver Neoplasms - metabolism Mesenchyme Metastases Metastasis MicroRNAs - genetics MicroRNAs - metabolism miRNA mRNA Overexpression Protein Kinases - genetics Protein Kinases - metabolism Repressor Proteins - genetics Repressor Proteins - metabolism Research Paper Restoration TOR protein Tumors |
| title | miR-424-5p represses the metastasis and invasion of intrahepatic cholangiocarcinoma by targeting ARK5 |
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