MiR-125b Suppression Inhibits Apoptosis and Negatively Regulates Sema4D in Avian Leukosis Virus-Transformed Cells
Subgroup J avian leukosis virus (ALV-J), an oncogenic retrovirus, causes hemangiomas and myeloid tumors in chickens. We previously showed that miR-125b is down-regulated in ALV-J-induced tumors. This study aimed to investigate the possible role of miR-125b in ALV-J-mediated infection and tumorigenes...
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MDPI AG
2019-08-01
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| Series: | Viruses |
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| Online Access: | https://www.mdpi.com/1999-4915/11/8/728 |
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| author | Chaoqi Ren Ruyu Xie Yongxiu Yao Mengmeng Yu Fangfang Chang Lixiao Xing Yao Zhang Yongzhen Liu Suyan Wang Muhammad Farooque Yongqiang Wang Xiaole Qi Changjun Liu Yanping Zhang Hongyu Cui Kai Li Li Gao Qing Pan Venugopal Nair Xiaomei Wang Yulong Gao |
| author_facet | Chaoqi Ren Ruyu Xie Yongxiu Yao Mengmeng Yu Fangfang Chang Lixiao Xing Yao Zhang Yongzhen Liu Suyan Wang Muhammad Farooque Yongqiang Wang Xiaole Qi Changjun Liu Yanping Zhang Hongyu Cui Kai Li Li Gao Qing Pan Venugopal Nair Xiaomei Wang Yulong Gao |
| author_sort | Chaoqi Ren |
| collection | DOAJ |
| description | Subgroup J avian leukosis virus (ALV-J), an oncogenic retrovirus, causes hemangiomas and myeloid tumors in chickens. We previously showed that miR-125b is down-regulated in ALV-J-induced tumors. This study aimed to investigate the possible role of miR-125b in ALV-J-mediated infection and tumorigenesis. Knockdown of miR-125b expression in HP45 cells reduced, whereas over-expression induced late-stage apoptosis. Bioinformatics analysis and luciferase activity assays indicate that miR-125b targets Semaphorin 4D/CD100 (Sema4D) by binding the 3′-untranslated region of messenger RNA (mRNA). Up-regulation of miR-125b in the DF1 cell line suppressed Sema4D expression, whereas miR-125 down-regulation increased Sema4D expression levels. To uncover the function of Sema4D during ALV-J infection, animal infection experiments and in vitro assays were performed and show that <i>Sema4D</i> mRNA levels were up-regulated in ALV-J-infected tissues and cells. Finally, functional experiments show that miR-125 down-regulation and Sema4D over-expression inhibited apoptosis in HP45 cells. These results suggest that miR-125b and its target Sema4D might play an important role in the aggressive growth of HP45 cells induced by avian leukosis viruses (ALVs). These findings improve our understanding of the underlying mechanism of ALV-J infection and tumorigenesis. |
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| id | doaj.art-132f57f6cbc34453b28574fa2de76f7b |
| institution | Directory Open Access Journal |
| issn | 1999-4915 |
| language | English |
| last_indexed | 2024-04-13T05:50:06Z |
| publishDate | 2019-08-01 |
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| record_format | Article |
| series | Viruses |
| spelling | doaj.art-132f57f6cbc34453b28574fa2de76f7b2022-12-22T02:59:49ZengMDPI AGViruses1999-49152019-08-0111872810.3390/v11080728v11080728MiR-125b Suppression Inhibits Apoptosis and Negatively Regulates Sema4D in Avian Leukosis Virus-Transformed CellsChaoqi Ren0Ruyu Xie1Yongxiu Yao2Mengmeng Yu3Fangfang Chang4Lixiao Xing5Yao Zhang6Yongzhen Liu7Suyan Wang8Muhammad Farooque9Yongqiang Wang10Xiaole Qi11Changjun Liu12Yanping Zhang13Hongyu Cui14Kai Li15Li Gao16Qing Pan17Venugopal Nair18Xiaomei Wang19Yulong Gao20Division of Avian Infectious Diseases, State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, Harbin 150069, ChinaDepartment of Life science, Northeast Forestry Universtiy, Harbin 150069, ChinaThe Pirbright Institute & UK-China Centre of Excellence for Research on Avian Diseases, Pirbright, Ash Road, Guildford, Surrey GU24 0NF, UKDivision of Avian Infectious Diseases, State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, Harbin 150069, ChinaDivision of Avian Infectious Diseases, State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, Harbin 150069, ChinaDivision of Avian Infectious Diseases, State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, Harbin 150069, ChinaDivision of Avian Infectious Diseases, State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, Harbin 150069, ChinaDivision of Avian Infectious Diseases, State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, Harbin 150069, ChinaDivision of Avian Infectious Diseases, State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, Harbin 150069, ChinaDivision of Avian Infectious Diseases, State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, Harbin 150069, ChinaDivision of Avian Infectious Diseases, State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, Harbin 150069, ChinaDivision of Avian Infectious Diseases, State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, Harbin 150069, ChinaDivision of Avian Infectious Diseases, State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, Harbin 150069, ChinaDivision of Avian Infectious Diseases, State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, Harbin 150069, ChinaDivision of Avian Infectious Diseases, State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, Harbin 150069, ChinaDivision of Avian Infectious Diseases, State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, Harbin 150069, ChinaDivision of Avian Infectious Diseases, State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, Harbin 150069, ChinaDivision of Avian Infectious Diseases, State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, Harbin 150069, ChinaThe Pirbright Institute & UK-China Centre of Excellence for Research on Avian Diseases, Pirbright, Ash Road, Guildford, Surrey GU24 0NF, UKDivision of Avian Infectious Diseases, State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, Harbin 150069, ChinaDivision of Avian Infectious Diseases, State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, Harbin 150069, ChinaSubgroup J avian leukosis virus (ALV-J), an oncogenic retrovirus, causes hemangiomas and myeloid tumors in chickens. We previously showed that miR-125b is down-regulated in ALV-J-induced tumors. This study aimed to investigate the possible role of miR-125b in ALV-J-mediated infection and tumorigenesis. Knockdown of miR-125b expression in HP45 cells reduced, whereas over-expression induced late-stage apoptosis. Bioinformatics analysis and luciferase activity assays indicate that miR-125b targets Semaphorin 4D/CD100 (Sema4D) by binding the 3′-untranslated region of messenger RNA (mRNA). Up-regulation of miR-125b in the DF1 cell line suppressed Sema4D expression, whereas miR-125 down-regulation increased Sema4D expression levels. To uncover the function of Sema4D during ALV-J infection, animal infection experiments and in vitro assays were performed and show that <i>Sema4D</i> mRNA levels were up-regulated in ALV-J-infected tissues and cells. Finally, functional experiments show that miR-125 down-regulation and Sema4D over-expression inhibited apoptosis in HP45 cells. These results suggest that miR-125b and its target Sema4D might play an important role in the aggressive growth of HP45 cells induced by avian leukosis viruses (ALVs). These findings improve our understanding of the underlying mechanism of ALV-J infection and tumorigenesis.https://www.mdpi.com/1999-4915/11/8/728miR-125bSubgroup J avian leukosis virusSema4Dcell apoptosis |
| spellingShingle | Chaoqi Ren Ruyu Xie Yongxiu Yao Mengmeng Yu Fangfang Chang Lixiao Xing Yao Zhang Yongzhen Liu Suyan Wang Muhammad Farooque Yongqiang Wang Xiaole Qi Changjun Liu Yanping Zhang Hongyu Cui Kai Li Li Gao Qing Pan Venugopal Nair Xiaomei Wang Yulong Gao MiR-125b Suppression Inhibits Apoptosis and Negatively Regulates Sema4D in Avian Leukosis Virus-Transformed Cells Viruses miR-125b Subgroup J avian leukosis virus Sema4D cell apoptosis |
| title | MiR-125b Suppression Inhibits Apoptosis and Negatively Regulates Sema4D in Avian Leukosis Virus-Transformed Cells |
| title_full | MiR-125b Suppression Inhibits Apoptosis and Negatively Regulates Sema4D in Avian Leukosis Virus-Transformed Cells |
| title_fullStr | MiR-125b Suppression Inhibits Apoptosis and Negatively Regulates Sema4D in Avian Leukosis Virus-Transformed Cells |
| title_full_unstemmed | MiR-125b Suppression Inhibits Apoptosis and Negatively Regulates Sema4D in Avian Leukosis Virus-Transformed Cells |
| title_short | MiR-125b Suppression Inhibits Apoptosis and Negatively Regulates Sema4D in Avian Leukosis Virus-Transformed Cells |
| title_sort | mir 125b suppression inhibits apoptosis and negatively regulates sema4d in avian leukosis virus transformed cells |
| topic | miR-125b Subgroup J avian leukosis virus Sema4D cell apoptosis |
| url | https://www.mdpi.com/1999-4915/11/8/728 |
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