%0 Generic %A V., Nalini %A P.R., Deepa %A R., Raguraman %A V., Khetan %A M.A., Reddy %A S., Krishnakumar %D 2016 %T Supplementary Material for: Targeting HMGA2 in Retinoblastoma Cells in vitro Using the Aptamer Strategy %U https://karger.figshare.com/articles/dataset/Supplementary_Material_for_Targeting_HMGA2_in_Retinoblastoma_Cells_in_vitro_Using_the_Aptamer_Strategy/3468911 %R 10.6084/m9.figshare.3468911.v1 %2 https://karger.figshare.com/ndownloader/files/5460629 %2 https://karger.figshare.com/ndownloader/files/5460632 %K •HMGA2 %K •HMGA2-aptamer %K TGFβ-SMAD4 %K •Retinoblastoma %K •Etoposide %X 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 TGFβ, SMAD4, CDH1, BAX, CASP 3, PARP mRNA and decreased SNAI1, Bcl2 mRNA levels in aptamer-treated RB cells suggests the activation of TGFβ-SMAD4-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. %I Karger Publishers