AI Article Synopsis
- HC11 cells are a type of mouse mammary cell that stay normal, while HC11 ras cells, which have been transformed with the H-ras gene, can cause tumors.
- The study found that HC11 ras cells have less Vitamin D receptor (VDR) mRNA, but this is not because of differences in how the gene is transcribed.
- Instead, the lower VDR mRNA levels in HC11 ras cells are likely due to increased degradation after transcription, and blocking the ras pathway can restore VDR mRNA levels.
Article Abstract
HC11, a spontaneously immortalized murine mammary lineage maintains features of normal cells while HC11 H-ras transformed cells (HC11 ras) are tumorigenic. Ras transformation is associated with a lower Vitamin D receptor (VDR) mRNA content. Our goal was to investigate the mechanism underlying VDR mRNA differences between these cells. Although the VDR transcriptional rate measured by run-on assays did not differ between the cells, our data suggested a pos transcriptional mechanism involving higher VDR mRNA degradation in HC11 ras cells which was not due to mutations in its 3'-UTR region since sequences of mRNA obtained from HC11 and HC11 ras cells were identical. Treatment of HC11 ras cells with a farnesyltransferase inhibitor, which prevents ras activation, causing an enhancement of VDR mRNA levels, indicating an association between the ras signaling pathway and VDR mRNA instability. The present work suggests that the decreased mRNA levels in HC11 ras cells might in part be due to an early loss of stability.
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| http://dx.doi.org/10.1016/j.jsbmb.2004.05.007 | DOI Listing |
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