Unknown,Transcriptomics,Genomics,Proteomics

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Expression Analysis of Mammary Epithelial Cells Isolated from 12-16 Week Old Virgin C57Bl6 Lrp5+/+ and Lrp5-/- Mice

ABSTRACT: Investigation of whole-genome gene expression level changes in C57Bl6 Lrp5-/- mammary epithelial cells, compared to the wild-type strain. The mammary epithelial cells were isolated from numbers 4 and 5 mammary glands. The Lrp5-/- mouse strain described in this study has been further described in Lindvall C, Evans NC, Zylstra CR, Li Y, Alexander CM, Williams BO. 2006. The Wnt signaling receptor Lrp5 is required for mammary ductal stem cell activity and Wnt1-induced tumorigenesis. J Biol Chem. 2006 Nov 17;281(46):35081-7. Epub 2006 Sep 13. PMID: 16973609. Mammary epithelial cells were isolated from 6 groups of Lrp5+/+ and 3 groups of Lrp5-/- mice. The isolated RNA was submitted to the Gene Expression Center, University of Wisconsin-Madison where it was labelled with Cy3. Labelled samples were submitted to Roche Nimblegen and were hybridized to Mus musculus 1-Plex arrays that represent 42,586 mouse genes.

ORGANISM(S): Mus musculus

SUBMITTER: Caroline Alexander

PROVIDER: E-GEOD-19228 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Identify gene expression changes in the absence of Plk2 Disruptions in polarity and mitotic spindle orientation contribute to the progression and evolution of tumorigenesis. However, little is known about the molecular mechanisms regulating these processes in vivo. Here we demonstrate that Polo-like kinase 2 (Plk2) regulates mitotic spindle orientation in the mammary gland and is a putative tumor suppressor. Plk2 is highly expressed in the mammary gland and is required for proper mammary gland development. Loss of Plk2 leads to increased mammary epithelial cell proliferation and ductal hyperbranching. Additionally a novel role for Plk2 in regulating the orientation of the mitotic spindle and maintaining proper cell polarity in the ductal epithelium was discovered. In support of a tumor suppressor function for Plk2, loss of Plk2 increased the formation of lesions in multiparous glands. Collectively, these results demonstrate a novel role for Plk2 in regulating mammary gland development and as a tumor suppressor in mammary tumorigenesis. Disruptions in polarity and mitotic spindle orientation contribute to the progression and evolution of tumorigenesis. However, little is known about the molecular mechanisms regulating these processes in vivo. Here we demonstrate that Polo-like kinase 2 (Plk2) regulates mitotic spindle orientation in the mammary gland and is a putative tumor suppressor. Plk2 is highly expressed in the mammary gland and is required for proper mammary gland development. Loss of Plk2 leads to increased mammary epithelial cell proliferation and ductal hyperbranching. Additionally a novel role for Plk2 in regulating the orientation of the mitotic spindle and maintaining proper cell polarity in the ductal epithelium was discovered. In support of a tumor suppressor function for Plk2, loss of Plk2 increased the formation of lesions in multiparous glands. Collectively, these results demonstrate a novel role for Plk2 in regulating mammary gland development and as a tumor suppressor in mammary tumorigenesis. Comparison between Plk2 +/+ (n=3) and Plk2 -/- (n=3) mouse mammary epithelial cells

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Expression Analysis of Mammary Epithelial Cells Isolated from 12-16 Week Old Virgin C57Bl6 Lrp5+/+ and Lrp5-/- Mice

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