A herpes simplex virus type 2-encoded microRNA promotes tumor cell metastasis by targeting suppressor of cytokine signaling 2 in lung cancer
Autor: | Hongli Yan, Xudong Wang, Shupeng Liu, Zhou Zhenhua, Jianru Xiao |
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Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
Male Lung Neoplasms Herpesvirus 2 Human Bone Neoplasms Suppressor of Cytokine Signaling Proteins Biology medicine.disease_cause Metastasis 03 medical and health sciences 0302 clinical medicine Cell Line Tumor microRNA medicine Humans Neoplasm Metastasis Lung cancer SOCS2 RC254-282 Aged Cell Proliferation Suppressor of cytokine signaling 1 Neoplasms. Tumors. Oncology. Including cancer and carcinogens Bone metastasis General Medicine Middle Aged medicine.disease Gene Expression Regulation Neoplastic MicroRNAs 030104 developmental biology Herpes simplex virus Real-time polymerase chain reaction 030220 oncology & carcinogenesis Immunology Cancer research Female |
Zdroj: | Tumor Biology, Vol 39 (2017) |
ISSN: | 1423-0380 |
Popis: | Certain viruses use microRNAs to regulate the expression of their own genes, host genes, or both. A number of microRNAs expressed by herpes simplex virus type 2 have been confirmed by previous studies. However, whether these microRNAs play a role in the metastasis of lung cancers and how these viral microRNAs precisely regulated the tumor biological process in lung cancer bone metastasis remain obscure. We recently identified the high expression of an acutely and latently expressed viral microRNA, Hsv2-miR-H9-5p, encoded by herpes simplex virus type 2 latency-associated transcript through microarray and quantitative polymerase chain reaction analyses which compared the expression of microRNAs in bone metastasis from lung cancer with primary lung cancers. We now reported that Hsv2-miR-H9-5p was highly expressed in bone metastasis and closely associated with pathological and metastatic processes of lung cancers. The functions of Hsv2-miR-H9-5p were determined by overexpression which results in an increase in survival, migration, and invasion of lung cancer cells in vitro. We determined that Hsv2-miR-H9-5p directly targeted SOCS2 mechanistically by dual-luciferase reporter assay. Then, we investigated the functions of SOCS2 in the progress of lung cancers. Reduction of SOCS2 dosage by hsv2-miR-H9-5p induced increased migration and invasion of lung cancer cells. Overexpression of SOCS2 inverted these phenotypes generated by hsv2-miR-H9-5p, indicating the potential roles of SOCS2 in Hsv2-miR-H9-5p-driven metastasis in lung cancers. The results highlighted that Hsv2-miR-H9-5p regulated and contributed to bone metastasis of lung cancers. We proposed that Hsv2-miR-H9-5p could be used as a potential target in lung cancer therapy. |
Databáze: | OpenAIRE |
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