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miR-374a-CCND1-pPI3K/AKT-c-JUN feedback loop modulated by PDCD4 suppresses cell growth, metastasis, and sensitizes nasopharyngeal carcinoma to cisplatin
miR-374a has been reported to function as an oncogene during tumor pathogenesis. In this study, miR-374a is observed to reduce nasopharyngeal carcinoma (NPC) cell proliferation, migration, invasion, metastasis and cisplatin (DDP) resistance in vitro and in vivo . Mechanistic analyses indicate that m...
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| Published in: | Oncogene 2017-01, Vol.36 (2), p.275-285 |
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| Main Authors: | , , , , , , , , , |
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| creator | Zhen, Y Fang, W Zhao, M Luo, R Liu, Y Fu, Q Chen, Y Cheng, C Zhang, Y Liu, Z |
| description | miR-374a has been reported to function as an oncogene during tumor pathogenesis. In this study, miR-374a is observed to reduce nasopharyngeal carcinoma (NPC) cell proliferation, migration, invasion, metastasis and cisplatin (DDP) resistance
in vitro
and
in vivo
. Mechanistic analyses indicate that miR-374a directly targets CCND1 to inactivate pPI3K/pAKT/c-JUN forming a negative feedback loop, as well as suppressing downstream signals related to cell cycle progression and epithelial−mesenchymal transition (EMT). Interestingly, we also observed that miR-374a direct targeting of CCND1 is modulated by tumor suppressor PDCD4 via suppressing pPI3K/pAKT/c-JUN signaling. In clinical specimens, miR-374a was positively and negatively correlated with expression of PDCD4 and CCND1, respectively. Our studies are the first to demonstrate that the miR-374a-CCND1-pPI3K/AKT-c-JUN feedback loop induced by PDCD4 supresses NPC cell growth, metastasis and chemotherapy resistance. |
| doi_str_mv | 10.1038/onc.2016.201 |
| format | article |
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in vitro
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. Mechanistic analyses indicate that miR-374a directly targets CCND1 to inactivate pPI3K/pAKT/c-JUN forming a negative feedback loop, as well as suppressing downstream signals related to cell cycle progression and epithelial−mesenchymal transition (EMT). Interestingly, we also observed that miR-374a direct targeting of CCND1 is modulated by tumor suppressor PDCD4 via suppressing pPI3K/pAKT/c-JUN signaling. In clinical specimens, miR-374a was positively and negatively correlated with expression of PDCD4 and CCND1, respectively. Our studies are the first to demonstrate that the miR-374a-CCND1-pPI3K/AKT-c-JUN feedback loop induced by PDCD4 supresses NPC cell growth, metastasis and chemotherapy resistance.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/onc.2016.201</identifier><identifier>PMID: 27270423</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/109 ; 13/31 ; 13/51 ; 14/35 ; 42/89 ; 45/61 ; 45/90 ; 59/5 ; 631/67/1059 ; 631/67/1536 ; 631/67/322 ; 631/67/581 ; 64 ; 64/60 ; 82/1 ; 82/80 ; 96/95 ; Animals ; Apoptosis ; Apoptosis Regulatory Proteins - genetics ; Cancer metastasis ; Carcinoma ; Carcinoma - drug therapy ; Carcinoma - genetics ; Carcinoma - metabolism ; Care and treatment ; Cell Biology ; Cell Cycle - drug effects ; Cell growth ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Chemotherapy ; Cisplatin - administration & dosage ; Cisplatin - pharmacology ; Cyclin D1 - genetics ; Development and progression ; Diagnosis ; Drug resistance ; Drug Resistance, Neoplasm ; Epithelial-Mesenchymal Transition - drug effects ; Feedback, Physiological ; Gene Expression Regulation, Neoplastic - drug effects ; Head & neck cancer ; Human Genetics ; Humans ; Internal Medicine ; Medicine ; Medicine & Public Health ; Mice ; MicroRNAs ; MicroRNAs - genetics ; Nasopharyngeal cancer ; Nasopharyngeal Carcinoma ; Nasopharyngeal Neoplasms - drug therapy ; Nasopharyngeal Neoplasms - genetics ; Nasopharyngeal Neoplasms - metabolism ; Neoplasm Metastasis ; Oncology ; original-article ; Phosphatidylinositol 3-Kinases - genetics ; Phosphatidylinositol 3-Kinases - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; RNA-Binding Proteins - genetics ; Signal Transduction - drug effects ; Tumorigenesis</subject><ispartof>Oncogene, 2017-01, Vol.36 (2), p.275-285</ispartof><rights>Macmillan Publishers Limited 2017</rights><rights>COPYRIGHT 2017 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jan 12, 2017</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3721-d489fb93fece6a756de28f7c3c8d4d062463b8b99ee66f4dd575fb39ea0682f33</citedby><cites>FETCH-LOGICAL-c3721-d489fb93fece6a756de28f7c3c8d4d062463b8b99ee66f4dd575fb39ea0682f33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27270423$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhen, Y</creatorcontrib><creatorcontrib>Fang, W</creatorcontrib><creatorcontrib>Zhao, M</creatorcontrib><creatorcontrib>Luo, R</creatorcontrib><creatorcontrib>Liu, Y</creatorcontrib><creatorcontrib>Fu, Q</creatorcontrib><creatorcontrib>Chen, Y</creatorcontrib><creatorcontrib>Cheng, C</creatorcontrib><creatorcontrib>Zhang, Y</creatorcontrib><creatorcontrib>Liu, Z</creatorcontrib><title>miR-374a-CCND1-pPI3K/AKT-c-JUN feedback loop modulated by PDCD4 suppresses cell growth, metastasis, and sensitizes nasopharyngeal carcinoma to cisplatin</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>miR-374a has been reported to function as an oncogene during tumor pathogenesis. In this study, miR-374a is observed to reduce nasopharyngeal carcinoma (NPC) cell proliferation, migration, invasion, metastasis and cisplatin (DDP) resistance
in vitro
and
in vivo
. Mechanistic analyses indicate that miR-374a directly targets CCND1 to inactivate pPI3K/pAKT/c-JUN forming a negative feedback loop, as well as suppressing downstream signals related to cell cycle progression and epithelial−mesenchymal transition (EMT). Interestingly, we also observed that miR-374a direct targeting of CCND1 is modulated by tumor suppressor PDCD4 via suppressing pPI3K/pAKT/c-JUN signaling. In clinical specimens, miR-374a was positively and negatively correlated with expression of PDCD4 and CCND1, respectively. Our studies are the first to demonstrate that the miR-374a-CCND1-pPI3K/AKT-c-JUN feedback loop induced by PDCD4 supresses NPC cell growth, metastasis and chemotherapy resistance.</description><subject>13/109</subject><subject>13/31</subject><subject>13/51</subject><subject>14/35</subject><subject>42/89</subject><subject>45/61</subject><subject>45/90</subject><subject>59/5</subject><subject>631/67/1059</subject><subject>631/67/1536</subject><subject>631/67/322</subject><subject>631/67/581</subject><subject>64</subject><subject>64/60</subject><subject>82/1</subject><subject>82/80</subject><subject>96/95</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis Regulatory Proteins - genetics</subject><subject>Cancer metastasis</subject><subject>Carcinoma</subject><subject>Carcinoma - drug therapy</subject><subject>Carcinoma - genetics</subject><subject>Carcinoma - metabolism</subject><subject>Care and treatment</subject><subject>Cell Biology</subject><subject>Cell Cycle - 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Academic</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhen, Y</au><au>Fang, W</au><au>Zhao, M</au><au>Luo, R</au><au>Liu, Y</au><au>Fu, Q</au><au>Chen, Y</au><au>Cheng, C</au><au>Zhang, Y</au><au>Liu, Z</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR-374a-CCND1-pPI3K/AKT-c-JUN feedback loop modulated by PDCD4 suppresses cell growth, metastasis, and sensitizes nasopharyngeal carcinoma to cisplatin</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2017-01-12</date><risdate>2017</risdate><volume>36</volume><issue>2</issue><spage>275</spage><epage>285</epage><pages>275-285</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>miR-374a has been reported to function as an oncogene during tumor pathogenesis. In this study, miR-374a is observed to reduce nasopharyngeal carcinoma (NPC) cell proliferation, migration, invasion, metastasis and cisplatin (DDP) resistance
in vitro
and
in vivo
. Mechanistic analyses indicate that miR-374a directly targets CCND1 to inactivate pPI3K/pAKT/c-JUN forming a negative feedback loop, as well as suppressing downstream signals related to cell cycle progression and epithelial−mesenchymal transition (EMT). Interestingly, we also observed that miR-374a direct targeting of CCND1 is modulated by tumor suppressor PDCD4 via suppressing pPI3K/pAKT/c-JUN signaling. In clinical specimens, miR-374a was positively and negatively correlated with expression of PDCD4 and CCND1, respectively. Our studies are the first to demonstrate that the miR-374a-CCND1-pPI3K/AKT-c-JUN feedback loop induced by PDCD4 supresses NPC cell growth, metastasis and chemotherapy resistance.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>27270423</pmid><doi>10.1038/onc.2016.201</doi><tpages>11</tpages></addata></record> |
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| subjects | 13/109 13/31 13/51 14/35 42/89 45/61 45/90 59/5 631/67/1059 631/67/1536 631/67/322 631/67/581 64 64/60 82/1 82/80 96/95 Animals Apoptosis Apoptosis Regulatory Proteins - genetics Cancer metastasis Carcinoma Carcinoma - drug therapy Carcinoma - genetics Carcinoma - metabolism Care and treatment Cell Biology Cell Cycle - drug effects Cell growth Cell Line, Tumor Cell Proliferation - drug effects Chemotherapy Cisplatin - administration & dosage Cisplatin - pharmacology Cyclin D1 - genetics Development and progression Diagnosis Drug resistance Drug Resistance, Neoplasm Epithelial-Mesenchymal Transition - drug effects Feedback, Physiological Gene Expression Regulation, Neoplastic - drug effects Head & neck cancer Human Genetics Humans Internal Medicine Medicine Medicine & Public Health Mice MicroRNAs MicroRNAs - genetics Nasopharyngeal cancer Nasopharyngeal Carcinoma Nasopharyngeal Neoplasms - drug therapy Nasopharyngeal Neoplasms - genetics Nasopharyngeal Neoplasms - metabolism Neoplasm Metastasis Oncology original-article Phosphatidylinositol 3-Kinases - genetics Phosphatidylinositol 3-Kinases - metabolism Proto-Oncogene Proteins c-akt - metabolism RNA-Binding Proteins - genetics Signal Transduction - drug effects Tumorigenesis |
| title | miR-374a-CCND1-pPI3K/AKT-c-JUN feedback loop modulated by PDCD4 suppresses cell growth, metastasis, and sensitizes nasopharyngeal carcinoma to cisplatin |
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