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LncRNA DLX6-AS1 promotes laryngeal squamous cell carcinoma growth and invasion through regulating miR-376c.
Am J Transl Res 2019; 11(11):7009-7017AJ

Abstract

Accumulating evidence showed that lncRNAs play important roles in tumour development. Recently, a novel lncRNA DLX6-AS1 was found to be overexpressed in some tumors such as lung adenocarcinoma, renal cell carcinoma and hepatocellular carcinoma. However, the functional roles of DLX6-AS1 in laryngeal squamous cell carcinoma (LSCC) are still unclear. In the study, we showed that the expression level of DLX6-AS1 was upregulated in the LSCC samples compared to the noncancerous tissues. By using CCK-8 analysis, we demonstrated that knockdown expression of DLX6-AS1 suppressed the Hep2 cell growth. DLX6-AS1 knockdown inhibited the Hep2 cell cycle and invasion. MiR-376c was identified to have the complementary binding sites with the DLX6-AS1. By luciferase reporter assay, we indicated that overexpression of miR-376c inhibited the luciferase activity of wild-type DLX6-AS1, but it failed to suppress luciferase activity of mutated one. DLX6-AS1 knockdown enhanced the expression of miR-376c in the Hep2 cell. Moreover, we showed that the expression level of miR-376c was lower in the LSCC samples than in the noncancerous tissues and the expression of miR-376c was negatively correlated with expression of DLX6-AS1 in LSCC tissues. Ectopic expression of miR-376c suppressed cell proliferation, cycle and invasion of LSCC cell. DLX6-AS1 knockdown suppressed cell proliferation, cycle and invasion via regulating miR-376c expression. These data proved that lncRNA DLX6-AS1 might play as an oncogene in LSCC development and tumorigenesis.

Authors+Show Affiliations

Department of Otolaryngology, Head and Neck Surgery, Zhoukou Central Hospital Zhoukou 466000, Henan, China.Department of Otolaryngology, Head and Neck Surgery, The First Affiliated Hospital of Zhengzhou University Zhengzhou 450052, Henan, China.Department of Otorhinolaryngology, Affiliated Hospital of Guizhou Medical University Guiyang 550004, Guizhou, China.Department of Otolaryngology, Head and Neck Surgery, Zhoukou Central Hospital Zhoukou 466000, Henan, China.Department of Otolaryngology, Head and Neck Surgery, Zhoukou Central Hospital Zhoukou 466000, Henan, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31814904

Citation

Yang, Qingjun, et al. "LncRNA DLX6-AS1 Promotes Laryngeal Squamous Cell Carcinoma Growth and Invasion Through Regulating MiR-376c." American Journal of Translational Research, vol. 11, no. 11, 2019, pp. 7009-7017.
Yang Q, Sun J, Ma Y, et al. LncRNA DLX6-AS1 promotes laryngeal squamous cell carcinoma growth and invasion through regulating miR-376c. Am J Transl Res. 2019;11(11):7009-7017.
Yang, Q., Sun, J., Ma, Y., Zhao, C., & Song, J. (2019). LncRNA DLX6-AS1 promotes laryngeal squamous cell carcinoma growth and invasion through regulating miR-376c. American Journal of Translational Research, 11(11), pp. 7009-7017.
Yang Q, et al. LncRNA DLX6-AS1 Promotes Laryngeal Squamous Cell Carcinoma Growth and Invasion Through Regulating MiR-376c. Am J Transl Res. 2019;11(11):7009-7017. PubMed PMID: 31814904.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - LncRNA DLX6-AS1 promotes laryngeal squamous cell carcinoma growth and invasion through regulating miR-376c. AU - Yang,Qingjun, AU - Sun,Jin, AU - Ma,Yifei, AU - Zhao,Chunjie, AU - Song,Jijun, Y1 - 2019/11/15/ PY - 2019/07/25/received PY - 2019/09/01/accepted PY - 2019/12/10/entrez PY - 2019/12/10/pubmed PY - 2019/12/10/medline KW - DLX6-AS1 KW - Laryngeal squamous cell carcinoma KW - lncRNA KW - miR-376c SP - 7009 EP - 7017 JF - American journal of translational research JO - Am J Transl Res VL - 11 IS - 11 N2 - Accumulating evidence showed that lncRNAs play important roles in tumour development. Recently, a novel lncRNA DLX6-AS1 was found to be overexpressed in some tumors such as lung adenocarcinoma, renal cell carcinoma and hepatocellular carcinoma. However, the functional roles of DLX6-AS1 in laryngeal squamous cell carcinoma (LSCC) are still unclear. In the study, we showed that the expression level of DLX6-AS1 was upregulated in the LSCC samples compared to the noncancerous tissues. By using CCK-8 analysis, we demonstrated that knockdown expression of DLX6-AS1 suppressed the Hep2 cell growth. DLX6-AS1 knockdown inhibited the Hep2 cell cycle and invasion. MiR-376c was identified to have the complementary binding sites with the DLX6-AS1. By luciferase reporter assay, we indicated that overexpression of miR-376c inhibited the luciferase activity of wild-type DLX6-AS1, but it failed to suppress luciferase activity of mutated one. DLX6-AS1 knockdown enhanced the expression of miR-376c in the Hep2 cell. Moreover, we showed that the expression level of miR-376c was lower in the LSCC samples than in the noncancerous tissues and the expression of miR-376c was negatively correlated with expression of DLX6-AS1 in LSCC tissues. Ectopic expression of miR-376c suppressed cell proliferation, cycle and invasion of LSCC cell. DLX6-AS1 knockdown suppressed cell proliferation, cycle and invasion via regulating miR-376c expression. These data proved that lncRNA DLX6-AS1 might play as an oncogene in LSCC development and tumorigenesis. SN - 1943-8141 UR - https://www.unboundmedicine.com/medline/citation/31814904/LncRNA_DLX6_AS1_promotes_laryngeal_squamous_cell_carcinoma_growth_and_invasion_through_regulating_miR_376c_ L2 - https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/31814904/ DB - PRIME DP - Unbound Medicine ER -