Fig 2: LINC00511/miR-195-5p/GCNT3 axis was identified to be a potential regulator in lung cancer via a ceRNA network. A. Common upregulated lncRNAs in LUAD and LUSC compared with normal non-tumor samples were screened by GEPIA 2 with adj. P < 0.05 and logFC>1.5. LUAD: lung adenocarcinoma. LUSC: lung squamous cell carcinoma. B. The top 5 most significantly upregulated genes from GSE85841 were presented. GSE85841 is a mRNA microarray data of 8 LUAD and adjacent non-tumor samples to screen the upregulated genes with P < 0.05 and logFC> = 1.5. C-G. The expression of the 5 genes in LUAD and LUSC. Data obtained from GEPIA database. H. The candidate miRNAs that link LINC00511 and GCNT3 mRNA were overlapped by Venny 2.1.0. The targets of LINC00511 and GCNT3 mRNA were both predicted using starbase algorithm

Fig 3: GCNT3 was the target gene of miR-195-5p. A The schematic diagram presents the complementary binding sites within GCNT3 and miR-195-5p. B Luciferase reporter assay confirmed the molecular binding. **P < 0.001 compared with WT + NC. #P < 0.05 compared with WT + mimic. C The expression of GCNT3 was detected by qRT-PCR assay in cancer tissues and normal tissues. **P < 0.001. D Pearson analysis was used to analyze the expression of GCNT3 and miR-195-5p in cancer tissues. E The expression of GCNT3 was detected by qRT-PCR assay in A549, PC9 and BEAS-2B cells. **P < 0.001 compared with BEAS-2B. F The GCNT3 mRNA expression were detected by qRT-PCR assay in A549 and PC9 cells transfected with si-lnc for 48 h. G The GCNT3 protein expression were detected by western blot assay in A549 and PC9 cells transfected with si-lnc for 48 h. H The GCNT3 protein expression were detected by western blot assay in A549 and PC9 cells transfected with si-GCNT3 or inhibitor for 48 h. **P < 0.001 compared with si-NC group. $$P < 0.001 compared with inhibitor-NC. ##P < 0.001 compared with si-GCNT3 + inhibitor. si-GCNT3, siRNA of GCNT3. si-NC, negative control of siRNA. inhibitor, miR-195-5p inhibitor. inhibitor-NC, negative control of inhibitor. si-GCNT3 + inhibitor, siRNA of GCNT3 + miR-195-5p inhibitor

Fig 4: GCNT3 silencing reversed the effect of miR-195-5p on the p metastasis of LUAD cells. A Migration capacity was determined by wound healing assay in A549 and PC9 cells transfected with si-GCNT3 or inhibitor for 48 h. B Cell invasion ability was detected by transwell invasion assay in A549 and PC9 cells transfected with si-GCNT3 or inhibitor for 48 h. **P < 0.001 compared with si-NC group. $$P < 0.001 compared with inhibitor-NC. ##P < 0.001 compared with si-GCNT3 + inhibitor. si-GCNT3, siRNA of GCNT3. si-NC, negative control of siRNA. inhibitor, miR-195-5p inhibitor. inhibitor-NC, negative control of inhibitor. si-GCNT3 + inhibitor, siRNA of GCNT3 + miR-195-5p inhibitor

Fig 5: The expression of GCNT3 is upregulated in BRCA tissues and cells. (A) Western blot analysis of GCNT3 expression in paired breast cancer tumors (T) and adjacent non-tumor tissues (N) from 7 patients. Left: GCNT3 expression and β-protein blotting of actin control. Right image: GCNT3 expression as quantified and analyzed in paired Student’s t-tests. (B) GCNT3 was found to be expressed in the cytoplasm via immunohistochemistry. (C) After sh-GCNT3 was used to interfere with breast cancer cells, the expression level of GCNT3 was significantly reduced. **, P<0.01. BRCA, breast cancer; NC, negative control.