Xiangyu Fan1, Yingying Sun2, Xu Guo1, Chunbo He1, Beiqiu Han1, Xilin Sun2. 1. Department of Radiation Oncology, The Fourth Hospital of Harbin Medical University, Haerbin, Heilongjiang, China. 2. TOF-PET/CT/MR Center, The Fourth Hospital of Harbin Medical University, Haerbin, Heilongjiang, China.
Abstract
BACKGROUND: Lung squamous cell carcinoma (LUSC) is a kind of lung cancer which possesses high morbidity and mortality. Long non-coding RNAs (lncRNAs) have been abundantly reported to participate in regulating cellular activities of various diseases, including cancers. LINC01116 was reported as a tumor promoter in some cancers, whereas its function has not been clarified in LUSC. OBJECTIVE: This exploration aimed to study the modulatory role of LINC01116 in LUSC. METHODS: The expressions of LINC01116, miR-744-5p and SCN1B were determined by RT-qPCR. CCK-8, EdU and transwell assays were conducted to evaluate the proliferative, migratory and invasive abilities of A549 and H1299 cells. The protein expression of SCN1B or EMT-associated proteins was examined through western blot assay. The interaction between miR-744-5p and LINC01116 (or SCN1B) was confirmed by RNA pull down and luciferase reporter assays. RESULTS: LINC01116 was up-regulated in LUSC tissues and cells, and LINC01116 repression limited the proliferative, migratory, invasive capabilities and EMT process in LUSC cells. In mechanism, LINC01116 directly interacted with miR-744-5p, and its expression was negatively correlated with miR-744-5p expression. SCN1B, overexpressed in LUSC tissues and cells, was proved to be targeted by miR-744-5p. Furthermore, SCN1B expression was in a negative association with miR-744-5p expression. At last, SCN1B amplification recovered the inhibitive effect of LINC01116 knockdown on cell proliferation, migration, invasion and EMT process in LUSC. CONCLUSION: LINC01116 regulated miR-744-5p/SCN1B axis to exacerbate LUSC, providing a helpful theoretic basis for the exploration of LUSC treatment.
BACKGROUND:Lung squamous cell carcinoma (LUSC) is a kind of lung cancer which possesses high morbidity and mortality. Long non-coding RNAs (lncRNAs) have been abundantly reported to participate in regulating cellular activities of various diseases, including cancers. LINC01116 was reported as a tumor promoter in some cancers, whereas its function has not been clarified in LUSC. OBJECTIVE: This exploration aimed to study the modulatory role of LINC01116 in LUSC. METHODS: The expressions of LINC01116, miR-744-5p and SCN1B were determined by RT-qPCR. CCK-8, EdU and transwell assays were conducted to evaluate the proliferative, migratory and invasive abilities of A549 and H1299 cells. The protein expression of SCN1B or EMT-associated proteins was examined through western blot assay. The interaction between miR-744-5p and LINC01116 (or SCN1B) was confirmed by RNA pull down and luciferase reporter assays. RESULTS:LINC01116 was up-regulated in LUSC tissues and cells, and LINC01116 repression limited the proliferative, migratory, invasive capabilities and EMT process in LUSC cells. In mechanism, LINC01116 directly interacted with miR-744-5p, and its expression was negatively correlated with miR-744-5p expression. SCN1B, overexpressed in LUSC tissues and cells, was proved to be targeted by miR-744-5p. Furthermore, SCN1B expression was in a negative association with miR-744-5p expression. At last, SCN1B amplification recovered the inhibitive effect of LINC01116 knockdown on cell proliferation, migration, invasion and EMT process in LUSC. CONCLUSION:LINC01116 regulated miR-744-5p/SCN1B axis to exacerbate LUSC, providing a helpful theoretic basis for the exploration of LUSC treatment.