Targeting HMGA2 in Retinoblastoma Cells in vitro Using the Aptamer Strategy

Please use this identifier to cite or link to this item: http://dspace.bits-pilani.ac.in:8080/jspui/handle/123456789/2097

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DC Field	Value	Language
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
Appears in Collections:	Department of Biological Sciences

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