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Targeting HMGA2 in Retinoblastoma Cells in vitro Using the Aptamer Strategy

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dc.contributor.author Deepa, P.R.
dc.date.accessioned 2021-09-17T04:44:36Z
dc.date.available 2021-09-17T04:44:36Z
dc.date.issued 2016
dc.identifier.uri https://www.karger.com/Article/Fulltext/447300
dc.identifier.uri http://dspace.bits-pilani.ac.in:8080/xmlui/handle/123456789/2097
dc.description.abstract 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. en_US
dc.language.iso en en_US
dc.publisher Karger en_US
dc.subject Biology en_US
dc.subject HMGA2-aptamer en_US
dc.subject TGFβ-SMAD4 en_US
dc.subject Retinoblastoma en_US
dc.title Targeting HMGA2 in Retinoblastoma Cells in vitro Using the Aptamer Strategy en_US
dc.type Article en_US


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