Aberrant Expression of miR-362 Promotes Lung Cancer Metastasis through Downregulation of Sema3A
miR-362 is a recently discovered member of the microRNA family, and it modulates a variety of physical activities and plays an important role in the occurrence and development of many tumors. However, the biological functions of hsa-miR-362-5p in non-small-cell lung carcinoma (NSCLC) are unknown. Tr...
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| Main Authors: | , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2018-01-01
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| Series: | Journal of Immunology Research |
| Online Access: | http://dx.doi.org/10.1155/2018/1687097 |
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| author | Dan Luo Zheng Zhang Zhao Zhang Jia-Yue Li Jian Cui Wen-Pu Shi Xi-Wen Dong Lin Yuan Peng Lin Zhi-Nan Chen Hui-Jie Bian Zi-Ling Wang |
| author_facet | Dan Luo Zheng Zhang Zhao Zhang Jia-Yue Li Jian Cui Wen-Pu Shi Xi-Wen Dong Lin Yuan Peng Lin Zhi-Nan Chen Hui-Jie Bian Zi-Ling Wang |
| author_sort | Dan Luo |
| collection | DOAJ |
| description | miR-362 is a recently discovered member of the microRNA family, and it modulates a variety of physical activities and plays an important role in the occurrence and development of many tumors. However, the biological functions of hsa-miR-362-5p in non-small-cell lung carcinoma (NSCLC) are unknown. Transwell assay and colony formation were used to determine the migration, invasion, and proliferation of NSCLC cells in vitro. A subcutaneous tumor model in nude mice was established to detect NSCLC tumor growth in vivo. The direct binding of miR-362 to the 3′UTR of Semaphorin 3A (Sema3A) was confirmed by luciferase reporter assay. In this study, we found that the level of miR-362 was higher in NSCLC tissues than in adjacent normal tissues and that the level of miR-362 expression was also elevated in five NSCLC cell lines (A549, 95-D, H1299, H292, and H460) relative to a human normal lung epithelial cell line (BEAS2B). Furthermore, miR-362 promoted NSCLC cell invasion, migration, and colony formation in vitro and tumor formation in vivo. Next, we identified the miR-362 target gene Sema3A, which is significantly correlated with metastasis. Sema3A expression was increased in normal tissues relative to NSCLC tissues. This result is consistent with the fact that miR-362 expression is negatively correlated with Sema3A expression in clinical tissue samples and indicated that miR-362 can regulate Sema3A expression in NSCLC cells and consequently affect NSCLC invasion, migration, and colony formation. Taken together, these findings on the newly identified miR-362/Sema3A axis elucidate the molecular mechanism of NSCLC invasion and migration and could lead to a potential therapeutic target in NSCLC treatment. |
| format | Article |
| id | doaj-art-79df04f963f14bc482f9c338b4ef5b20 |
| institution | Kabale University |
| issn | 2314-8861 2314-7156 |
| language | English |
| publishDate | 2018-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Journal of Immunology Research |
| spelling | doaj-art-79df04f963f14bc482f9c338b4ef5b202025-02-03T05:47:09ZengWileyJournal of Immunology Research2314-88612314-71562018-01-01201810.1155/2018/16870971687097Aberrant Expression of miR-362 Promotes Lung Cancer Metastasis through Downregulation of Sema3ADan Luo0Zheng Zhang1Zhao Zhang2Jia-Yue Li3Jian Cui4Wen-Pu Shi5Xi-Wen Dong6Lin Yuan7Peng Lin8Zhi-Nan Chen9Hui-Jie Bian10Zi-Ling Wang11College of Life Science and Bioengineering, School of Science, Beijing Jiaotong University, Beijing 100044, ChinaNational Translational Science Center for Molecular Medicine, Department of Cell Biology, School of Basic Medicine, Air Force Medical University, Xi’an 710032, ChinaNational Translational Science Center for Molecular Medicine, Department of Cell Biology, School of Basic Medicine, Air Force Medical University, Xi’an 710032, ChinaNational Translational Science Center for Molecular Medicine, Department of Cell Biology, School of Basic Medicine, Air Force Medical University, Xi’an 710032, ChinaState Key Laboratory of Pharmaceutical Biotechnology and Collaborative Innovation Center of Chemistry for Life Sciences, School of Life Sciences, Nanjing University, Nanjing 210023, ChinaInstitute for Special Environmental Biophysics, Key Laboratory for Space Bioscience and Biotechnology, School of Life Sciences, Northwestern Polytechnical University, Xi'an 710072, ChinaNational Translational Science Center for Molecular Medicine, Department of Cell Biology, School of Basic Medicine, Air Force Medical University, Xi’an 710032, ChinaClinical Laboratory, No.457 Hospital of PLA, Wuhan 430000, ChinaNational Translational Science Center for Molecular Medicine, Department of Cell Biology, School of Basic Medicine, Air Force Medical University, Xi’an 710032, ChinaCollege of Life Science and Bioengineering, School of Science, Beijing Jiaotong University, Beijing 100044, ChinaNational Translational Science Center for Molecular Medicine, Department of Cell Biology, School of Basic Medicine, Air Force Medical University, Xi’an 710032, ChinaCollege of Life Science and Bioengineering, School of Science, Beijing Jiaotong University, Beijing 100044, ChinamiR-362 is a recently discovered member of the microRNA family, and it modulates a variety of physical activities and plays an important role in the occurrence and development of many tumors. However, the biological functions of hsa-miR-362-5p in non-small-cell lung carcinoma (NSCLC) are unknown. Transwell assay and colony formation were used to determine the migration, invasion, and proliferation of NSCLC cells in vitro. A subcutaneous tumor model in nude mice was established to detect NSCLC tumor growth in vivo. The direct binding of miR-362 to the 3′UTR of Semaphorin 3A (Sema3A) was confirmed by luciferase reporter assay. In this study, we found that the level of miR-362 was higher in NSCLC tissues than in adjacent normal tissues and that the level of miR-362 expression was also elevated in five NSCLC cell lines (A549, 95-D, H1299, H292, and H460) relative to a human normal lung epithelial cell line (BEAS2B). Furthermore, miR-362 promoted NSCLC cell invasion, migration, and colony formation in vitro and tumor formation in vivo. Next, we identified the miR-362 target gene Sema3A, which is significantly correlated with metastasis. Sema3A expression was increased in normal tissues relative to NSCLC tissues. This result is consistent with the fact that miR-362 expression is negatively correlated with Sema3A expression in clinical tissue samples and indicated that miR-362 can regulate Sema3A expression in NSCLC cells and consequently affect NSCLC invasion, migration, and colony formation. Taken together, these findings on the newly identified miR-362/Sema3A axis elucidate the molecular mechanism of NSCLC invasion and migration and could lead to a potential therapeutic target in NSCLC treatment.http://dx.doi.org/10.1155/2018/1687097 |
| spellingShingle | Dan Luo Zheng Zhang Zhao Zhang Jia-Yue Li Jian Cui Wen-Pu Shi Xi-Wen Dong Lin Yuan Peng Lin Zhi-Nan Chen Hui-Jie Bian Zi-Ling Wang Aberrant Expression of miR-362 Promotes Lung Cancer Metastasis through Downregulation of Sema3A Journal of Immunology Research |
| title | Aberrant Expression of miR-362 Promotes Lung Cancer Metastasis through Downregulation of Sema3A |
| title_full | Aberrant Expression of miR-362 Promotes Lung Cancer Metastasis through Downregulation of Sema3A |
| title_fullStr | Aberrant Expression of miR-362 Promotes Lung Cancer Metastasis through Downregulation of Sema3A |
| title_full_unstemmed | Aberrant Expression of miR-362 Promotes Lung Cancer Metastasis through Downregulation of Sema3A |
| title_short | Aberrant Expression of miR-362 Promotes Lung Cancer Metastasis through Downregulation of Sema3A |
| title_sort | aberrant expression of mir 362 promotes lung cancer metastasis through downregulation of sema3a |
| url | http://dx.doi.org/10.1155/2018/1687097 |
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