Research Paper Volume 14, Issue 4 pp 1782—1796

Long non-coding RNA Linc00205 promotes hepatoblastoma progression through regulating microRNA-154-3p/Rho-associated coiled-coil Kinase 1 axis via mitogen-activated protein kinase signaling

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Figure 6. Inhibition of miR-154-3p reversed changes in cell viability, colony formation ability, apoptosis, migration and invasion ability, caused by Linc00205 knockdown. (A) qRT-PCR assay for miR-154-3p expression among HepG2 cells transfected with si-Linc00205 and with or without miR-154-3p inhibitor. (B) Cell viability assay was carried out in HepG2 cells that were transfected with si-Linc00205 and with or without the miR-154-3p inhibitor. (C) Colony formation ability of HepG2 cells were transfected with si-Linc00205 and with or without miR-154-3p inhibitor. A quantitative analysis of colonies was performed (right panel). (D) Apoptosis assays of HepG2 cells transfected with si-Linc00205 and with or without miR-154-3p inhibitor, and quantitative analysis of the apoptosis cells (right panel). (E, F) The migration and invasion ability of HepG2 cells transfected with si-Linc00205 and with or without miR-154-3p inhibitor were determined through the use of a transwell migration assay (E) and transwell invasion assay (F) (left panel). A quantitative analysis of migratory or invasive cells in transwell assays was also performed (right panel). (G) Migration ability of HepG2 cells transfected with either si-Linc00205 and with or without miR-154-3p inhibitor at indicated time points was evaluated by wound healing assay (upper panel). The quantitative analysis of the gap of wound healing assay (lower panel) was performed at 48 hours. *p < 0.05.