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. 2009 Dec 24;4(12):e8445. doi: 10.1371/journal.pone.0008445

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This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration, which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

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(A) The miR-24-TS-SNP (829C→T) expressing CHO-DG44 cells over-expressed DHFR [22]. (B–C) DHFR over expression in CHO-DG44 cells due a loss of miR-24 function results in an increase in colony forming ability and (D) show anchorage-independent growth in semi solid agar as compared to vector alone expressing cells (p-value>0.05) (Soft agar colony-forming assay is abbreviated as SAC). (E) Transfection of a siRNA specific to DHFR reduced the ability of miR-24-TS-SNP expressing cells to form soft agar colonies by threefold. (F-H) miR-24-TS-SNP expression in a human cell line - MCF10A (G) and two rodent cell lines - NIH3T3 (H) and RK3 (see Table S1) resulted in more soft agar colony formation as compared to the cells expressing the vector alone and DHFR with wt 3′UTR. (I) DHFR overexpression due to the miR-24-TS-SNP renders NIH3T3 cells tumorigenic when transplanted in nude mice.