Mouse Gene Set: WANG_NEOPLASTIC_TRANSFORMATION_BY_CCND1_MYC

For the Human gene set with the same name, see WANG_NEOPLASTIC_TRANSFORMATION_BY_CCND1_MYC

Standard name WANG_NEOPLASTIC_TRANSFORMATION_BY_CCND1_MYC
Systematic name MM779
Brief description Selected genes changed in NMuMG cells (mammary epithelium) transformed by overexpression of CCND1 [GeneID=595] vs those transformed by overexpression of CCND1 and MYC [GeneID=4609].
Full description or abstract Cyclin D1 is one of the most commonly overexpressed oncogenes in breast cancer; yet, it is not clear whether cyclin D1 alone is capable of causing malignant transformation of mammary epithelial cells. Here, we show that ectopic expression of cyclin D1 in benign mouse mammary epithelial cells promotes cell proliferation, anchorage-independent growth in soft agar, and tumorigenesis in severe combined immunodeficient mice. To address the possible interaction of cyclin D1 and c-myc in malignant transformation, we used cyclin D1/c-myc dual-expressing clones, which displayed more aggressive and invasive phenotype than cyclin D1-expressing clones. These data provide evidence that overexpression of cyclin D1 or coexpression with c-myc could cause invasive malignant transformation of benign mouse mammary epithelial cells. Furthermore, microarray analysis of cyclin D1 and cyclin D1/c-myc clones showed that these two tumor-producing clones might use distinct invasive pathways. In summary, overexpression of cyclin D1 may commit mammary epithelia to a tumor-prone phenotype in which cooperation with other genes, such as synergy with c-myc, may lead to a more aggressive phenotype.
Collection M2: Curated
      CGP: Chemical and Genetic Perturbations
Source publication Pubmed 17440082   Authors: Wang Y,Thakur A,Sun Y,Wu J,Biliran H,Bollig A,Liao DJ
Exact source Table 3A
Related gene sets (show 8 gene sets from the same authors)
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Source species Mus musculus
Contributed by Jessica Robertson (MSigDB Team)
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identifier namespace		 MOUSE_SEQ_ACCESSION
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Version history 2022.1.Mm: First Introduced.

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