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LncRNA DLX6‐AS1 increases the expression of HIF‐1α and promotes the malignant phenotypes of nasopharyngeal carcinoma cells via targeting MiR‐199a‐5p

OBJECTIVE: To investigate the expression of long‐chain noncoding growth stasis specific protein 6 antisense RNA1 (lncRNA DLX6‐AS1) in nasopharyngeal carcinoma (NPC) tissues and cells, and its regulatory effect on malignant phenotypes of NPC cells. METHODS: The expressions of DLX6‐AS1, miR‐199a‐5p, a...

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Detalles Bibliográficos
Autores principales: Yang, Bin, Jia, Lin, Ren, Hui, Jin, Caibao, Ren, Qingrong, Zhang, Haiyuan, Hu, Desheng, Zhang, Hao, Hu, Liu, Xie, Tao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6978402/
https://www.ncbi.nlm.nih.gov/pubmed/31782911
http://dx.doi.org/10.1002/mgg3.1017
Descripción
Sumario:OBJECTIVE: To investigate the expression of long‐chain noncoding growth stasis specific protein 6 antisense RNA1 (lncRNA DLX6‐AS1) in nasopharyngeal carcinoma (NPC) tissues and cells, and its regulatory effect on malignant phenotypes of NPC cells. METHODS: The expressions of DLX6‐AS1, miR‐199a‐5p, and HIF‐1α mRNA in NPC issues and cells were detected by qRT‐PCR. The proliferation, metastasis, and invasion of cells were monitored via MTT and transwell assay. The interactions between DLX6‐AS1 and miR‐199a‐5p, miR‐199a‐5p and HIF‐1α were verified by luciferase activity assay. Western blot was performed to determine the regulatory effect of DLX6‐AS1 and miR‐199a‐5p on HIF‐1α protein. RESULTS: The expression of lncRNA DLX6‐AS1 was up‐regulated in NPC tissues and cells. The proliferation, migration, and invasion of NPC were enhanced by overexpressed DLX6‐AS1 but inhibited by DLX6‐AS1 knockdown. In addition, DLX6‐AS1 can be used as a kind of ceRNA to regulate miR‐199a‐5p and, thereby modulating the expression of HIF‐1α. CONCLUSION: We found that DLX6‐AS1 was a cancer‐promoting lncRNA to facilitate the progression of NPC, and its underlying mechanism was suppressing miR‐199a‐5p expression. This study can provide novel clues for the treatment of NPC.