European review for medical and pharmacological sciences · 2019
LINC01605 promotes the proliferation of laryngeal squamous cell carcinoma through targeting miR-493-3p.
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Wang X-Y, Wang L, Xu P-C, Huang F-J, Jian X, Wei Z-C, Chen Y-Q
Аннотация
OBJECTIVE: The purpose of this study was to elucidate the potential influence of LINC01605 on the progression of laryngeal squamous cell carcinoma (LSCC) and the underlying mechanism.
PATIENTS AND METHODS: LINC01605 and microRNA-493-3p (miR-493-3p) levels in normal laryngeal tissues, LSCC tissues, and paired paracancerous tissues were detected. Regulatory effects of LINC01605 on proliferative ability and apoptosis in HEp-2 and AMC-HN-8 cells were assessed. Besides, the interaction between LINC01605 and miR-493-3p was evaluated by Dual-Luciferase reporter gene assay and Spearman's rank correlation analysis. Finally, rescue experiments were conducted to clarify the role of LINC01605/miR-493-3p axis in the progression of LSCC.
RESULTS: LINC01605 was upregulated and miR-493-3p was downregulated in LSCC tissues. Knockdown of LINC01605 inhibited proliferative ability, and stimulated apoptosis in HEp-2 and AMC-HN-8 cells. Moreover, LINC01605 directly bound to miR-493-3p, and the former negatively regulated the level of the latter. In addition, miR-493-3p was able to reverse the regulatory effect of LINC01605 on proliferative ability in LSCC.
CONCLUSIONS: LINC01605 is upregulated in LSCC tissues, and it promotes the malignant progression of LSCC via targeting miR-493-3p.
PATIENTS AND METHODS: LINC01605 and microRNA-493-3p (miR-493-3p) levels in normal laryngeal tissues, LSCC tissues, and paired paracancerous tissues were detected. Regulatory effects of LINC01605 on proliferative ability and apoptosis in HEp-2 and AMC-HN-8 cells were assessed. Besides, the interaction between LINC01605 and miR-493-3p was evaluated by Dual-Luciferase reporter gene assay and Spearman's rank correlation analysis. Finally, rescue experiments were conducted to clarify the role of LINC01605/miR-493-3p axis in the progression of LSCC.
RESULTS: LINC01605 was upregulated and miR-493-3p was downregulated in LSCC tissues. Knockdown of LINC01605 inhibited proliferative ability, and stimulated apoptosis in HEp-2 and AMC-HN-8 cells. Moreover, LINC01605 directly bound to miR-493-3p, and the former negatively regulated the level of the latter. In addition, miR-493-3p was able to reverse the regulatory effect of LINC01605 on proliferative ability in LSCC.
CONCLUSIONS: LINC01605 is upregulated in LSCC tissues, and it promotes the malignant progression of LSCC via targeting miR-493-3p.