Supplementary Material for: Targeting HMGA2 in Retinoblastoma Cells in vitro Using the Aptamer Strategy

High-mobility group A2 (HMGA2) protein regulates retinoblastoma (RB) cancer cell proliferation. Here, a stable phosphorothioate-modified HMGA2 aptamer was used to block HMGA2 protein function in RB cells. HMGA2-aptamer internalisation in RB cells (Y79, Weri Rb1) and non-neoplastic human retinal cells (MIO-M1) were optimised. Aptamer induced dose-dependent cytotoxicity in RB cancer cells (0.25-1.5 µM). Increased expression of <i>TGFβ</i>, <i>SMAD4</i>,<i> CDH1</i>, <i>BAX</i>, <i>CASP 3</i>,<i> PARP </i>mRNA and decreased <i>SNAI1</i>,<i> Bcl2</i> mRNA levels in aptamer-treated RB cells suggests the activation of TGFβ-<i>SMAD4</i>-mediated apoptotic pathway. Synergistic effect with etoposide was observed in aptamer treated RB cells (p value ≤0.05). No significant toxicity was observed in non-neoplastic retinal cells.