Y Li1, J Xu, Y-N Guo, B-B Yang. 1. Department of Otorhinolaryngology, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China. yangbb1959@sina.com.
Abstract
OBJECTIVE: This study aims to investigate the expression level of long non-coding RNA (lncRNA) SNHG20 in laryngeal squamous cell carcinoma (LSCC), and to explore further whether it can promote the development of LSCC by regulating microRNA-140 (miR-140). PATIENTS AND METHODS: Expression levels of SNHG20 in 56 pairs of LSCC tissues and adjacent normal tissues were measured by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The relationship between SNHG20 expression with pathological parameters and the prognosis of LSCC was analyzed. Besides, the SNHG20 expression in LSCC cells was also analyzed by qRT-PCR. The SNHG20 knockdown and overexpression model were constructed by lentivirus transfection in AMC-HN-8 and Hep-2 cells. Cell counting kit-8 (CCK-8) and 5-Ethynyl-2'-deoxyuridine (EdU) assay were used to analyze the effect of SNHG20 on the biological function of LSCC cells. Finally, the dual-luciferase reporter gene assay was performed to explore the potentials of SNHG20 and miR-140 in LSCC. RESULTS: The SNHG20 expression in LSCC tissues or cells remarkably increased than controls, and the difference was statistically significant. The LSCC patients with the high expression level of SNHG20 were more likely to develop advanced tumor compared with patients with low expression of SNHG20. Moreover, the LSCC patients with the high expression level of SNHG20 had a shorter overall survival than those with low level. The cell proliferation ability significantly decreased in the SNHG20 knockdown group, while notably increased in SNHG20 overexpression group. MiR-140 was negatively correlated with SNHG20 in LSCC tissues and cells. Dual-luciferase reporter gene assay showed that SNHG20 could be targeted by miR-140 through a certain binding site. The cell rescue experiment also indicated that there was a mutual regulation between SNHG20 and miR-140, which could together affect the malignant progression of LSCC. CONCLUSIONS: We showed that the expression levels of SNHG20 in LSCC tissues or cell lines significantly increased and was associated with advanced tumor staging and undesirable prognosis of LSCC. In addition, SNHG20 could promote the malignant progression of LSCC.
OBJECTIVE: This study aims to investigate the expression level of long non-coding RNA (lncRNA) SNHG20 in laryngeal squamous cell carcinoma (LSCC), and to explore further whether it can promote the development of LSCC by regulating microRNA-140 (miR-140). PATIENTS AND METHODS: Expression levels of SNHG20 in 56 pairs of LSCC tissues and adjacent normal tissues were measured by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The relationship between SNHG20 expression with pathological parameters and the prognosis of LSCC was analyzed. Besides, the SNHG20 expression in LSCC cells was also analyzed by qRT-PCR. The SNHG20 knockdown and overexpression model were constructed by lentivirus transfection in AMC-HN-8 and Hep-2 cells. Cell counting kit-8 (CCK-8) and 5-Ethynyl-2'-deoxyuridine (EdU) assay were used to analyze the effect of SNHG20 on the biological function of LSCC cells. Finally, the dual-luciferase reporter gene assay was performed to explore the potentials of SNHG20 and miR-140 in LSCC. RESULTS: The SNHG20 expression in LSCC tissues or cells remarkably increased than controls, and the difference was statistically significant. The LSCC patients with the high expression level of SNHG20 were more likely to develop advanced tumor compared with patients with low expression of SNHG20. Moreover, the LSCC patients with the high expression level of SNHG20 had a shorter overall survival than those with low level. The cell proliferation ability significantly decreased in the SNHG20 knockdown group, while notably increased in SNHG20 overexpression group. MiR-140 was negatively correlated with SNHG20 in LSCC tissues and cells. Dual-luciferase reporter gene assay showed that SNHG20 could be targeted by miR-140 through a certain binding site. The cell rescue experiment also indicated that there was a mutual regulation between SNHG20 and miR-140, which could together affect the malignant progression of LSCC. CONCLUSIONS: We showed that the expression levels of SNHG20 in LSCC tissues or cell lines significantly increased and was associated with advanced tumor staging and undesirable prognosis of LSCC. In addition, SNHG20 could promote the malignant progression of LSCC.