Transcriptional knockdown of tumorigenic proteins inhibits the proliferation and migration of IMR-32 cells. (A) Transient siRNA transfection and knockdown of MYCN proto-oncogene, bHLH transcription factor (MYCN), L1-cell adhesion molecule (L1-CAM), high mobility group protein A1 (HMGA1) and fatty-acid binding protein 5 (FABP5) protein expression led to a significant decrease in IMR-32 cell proliferation from 48–96 h compared to the controls, as determined using a WST-1 cell proliferation assay. (B) Double-siRNA targeted knockdown (MYCN + L1-CAM, MYCN + HMGA1, MYCN + FABP5, L1-CAM + HMGA1, L1-CAM + FABP5 and HMGA1 + FABP5) also led to significant decrease in the IMR-32 cellular proliferation rate from 48–96 h compared to the controls. (C) Representative images of 'wound closure' illustrate a reduction in the migratory capacity of the IMR-32 cells subjected to FABP5 and HMGA1 siRNA knockdown. (D) The average area of 'wound closure' in multiple random fields, measured using AxioVision Systems software, revealed a statistically significant decrease in IMR-32 cell migration compared to the controls. Experiments were run in triplicate and repeated >3 times. Results represent the means ± SEM; *P<0.05.