Fig 2: Recovery of HMGA2 expression reverses inhibitory actions of si-VPS9D1-AS1 on NSCLC cells. (A) Quantification of HMGA2 protein expression in H460 and A549 cells transfected with plasmid pc-HMGA2 or the empty pcDNA3.1 vector along with si-VPS9D1-AS1 by western blot. *P < 0.05 vs. the si-NC group. #P < 0.05 vs. the si-VPS9D1-AS1 + pcDNA3.1 group. (B–F) Cell proliferation, colony formation, apoptosis, migration, and invasiveness parameters of H460 and A549 cells, treated as described above, determined by the CCK-8 assay, the colony formation assay, flow cytometry, and Transwell migration and invasiveness assays, respectively. *P < 0.05 vs. the si-NC group. #P < 0.05 vs. the si-VPS9D1-AS1 + pcDNA3.1 group.

Fig 3: MiR-205-5p/HMGA2 axis was involved in the regulation of HG-induced DN progression. A The overexpression effect of HMGA2 transfection on the HMGA2 protein expression was analyzed using western blot. B HMGA2 protein detection was performed by western blot in control, HG, HG + miR-NC, HG + miR-205-5p, HG + miR-205-5p + pcDNA or HG + miR-205-5p + HMGA2 group. C CCK-8 was used for the examination of cell viability. D ELISA was used for the determination of IL-6 and TNF-α. E EdU assay was used for the analysis of cell proliferation. F, G Western blot was applied for the protein measurement of collagen I and collagen IV. H, I SOD activity (G) and MDA level (H) by the respective kits were applied for the assessment of oxidative stress. **P < 0.01, ***P < 0.001, ****P < 0.0001

Fig 4: Elevation output of the miR-511-3p/HMGA2 axis abrogates the effects of LINC02163 knockdown in the malignant properties of breast cancer cells. (A, B) miR-511-3p inhibitor or NC inhibitor was introduced to MDA-MB-231 and MCF-7 cells in the presence of si-LINC02163. CCK-8 assay and flow cytometry were used to examine cell proliferation and apoptosis. (C, D) Migration and invasion of MDA-MB-231 and MCF-7 cells treated as described above were analyzed using Transwell cell migration and invasion assays. (E) The protein level of HMGA2 in MDA-MB-231 and MCF-7 cells following transfection of pc-HMGA2 or pcDNA3.1 was measured using Western blotting. (F–I) si-LINC02163 in combination with pc-HMGA2 or pcDNA3.1 was transfected into MDA-MB-231 and MCF-7 cells. After transfection, cell proliferation, apoptosis, migration, and invasion were analyzed using CCK-8 assay, flow cytometry, and Transwell cell migration and invasion assays, respectively. *p < 0.05 and **p < 0.01.

Fig 5: LINC00466 knockdown suppresses TSCC growth in vivo. (A) SCC-15 cells were stably transduced with lentivirus expressing either sh-LINC00466 or sh-NC. RT-qPCR analysis confirmed the successful LINC00466 knockdown in SCC-15 cells. (B) SCC-15 cells stably expressing sh-LINC00466 or sh-NC were injected into nude mice. Tumor xenograft volumes were measured every 3 days until 30 days following cell inoculation. (C) Tumor xenografts representative images collected from groups ‘sh-LINC00466' and ‘sh-NC’. (D) All the mice were euthanized 30 days after cell injection. The tumor xenografts were resected and weighed. (E) miR-493 levels in the tumor xenografts were measured via RT-qPCR. (F and G) The mRNA and protein levels of HMGA2 were determined in the tumor xenografts by respectively RT-qPCR and Western blot analysis. **P < 0.01.