Proteomic analysis of mouse mammary terminal end buds identifies axonal growth cone proteins

Morris, Joanna S.; Davies, Claire; Griffiths, Meryl; Pagé, Martin; Bruce, James A.; Patel, T.P.; Herath, Athula; Gusterson, Barry A.

doi:10.1002/pmic.200300699

Cited by 9 publications

(10 citation statements)

References 45 publications

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“…PCNA has been shown to be dramatically increased in terminal end buds (TEBs) by proteomic approaches. 43 As predicted, our results directly show the upregulation of PCNA in these estrogen-induced Cav-1 Ϫ/Ϫ mammary lesions ( Figure 8A). Similar results were obtained with an antibody directed against phospho-RB (Ser 807/811), another established marker of cell cycle progression ( Figure 8B).…”

Section: Cav-1 ϫ/ϫ Mammary Lesions Are Hyperproliferative Contain Masupporting

confidence: 63%

Genetic Ablation of Caveolin-1 Drives Estrogen-Hypersensitivity and the Development of DCIS-Like Mammary Lesions

Mercier

Casimiro

Zhou

et al. 2009

The American Journal of Pathology

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Caveolin-1 (Cav-1) loss-of-function mutations are exclusively associated with estrogen receptor-positive (ER(؉)) human breast cancers. To dissect the role of Cav-1 loss-of-function in the pathogenesis of human breast cancers, we used Cav-1 ؊/؊ null mice as a model system. First, we demonstrated that Cav-1 ؊/؊ mammary epithelia overexpress two well-established ER co-activator genes, CAPER and Foxa1, in addition to ER-␣. Thus, the functional loss of Cav-1 may be sufficient to confer estrogen-hypersensitivity in the mammary gland. To test this hypothesis directly, we subjected Cav-1 ؊/؊ mice to ovariectomy and estrogen supplementation. As predicted, Cav-1 ؊/؊ mammary glands were hyper-responsive to estrogen and developed dysplastic mammary lesions with adjacent stromal angiogenesis that resemble human ductal carcinoma in situ. Estrogen receptor signaling is tightly linked to the pathogenesis of human breast cancers. Estrogen receptor ␣ (ER-␣) is a ligand-activated transcription factor, which on the binding of the proper nuclear co-activators, initiatesSupported by grants from the NIH/NCI

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Section: Cav-1 ϫ/ϫ Mammary Lesions Are Hyperproliferative Contain Masupporting

confidence: 63%

Genetic Ablation of Caveolin-1 Drives Estrogen-Hypersensitivity and the Development of DCIS-Like Mammary Lesions

Mercier

Casimiro

Zhou

et al. 2009

The American Journal of Pathology

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“…TEB isolation was performed as described previously (Morris et al, 2004), with some modifications. MGs (#3–#5) were surgically isolated form adjacent tissues, minced into 1–2 mm pieces, and digested for 1 hr at 37°C in DMEM/F12 containing 5% FBS, 300 U/ml collagenase (Sigma-Aldrich), and 100 U/ml hyaluronidase (Sigma-Aldrich) with continuous shaking at 200 rpm and thorough mixing every 15 min.…”

Section: Methodsmentioning

confidence: 99%

Mammary Morphogenesis and Regeneration Require the Inhibition of EMT at Terminal End Buds by Ovol2 Transcriptional Repressor

et al. 2014

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SUMMARY Epithelial cells possess remarkable plasticity, having the ability to become mesenchymal cells through alterations in adhesion and motility (epithelial-to-mesenchymal transition [EMT]). However, how epithelial plasticity is kept in check in epithelial cells during tissue development and regeneration remains to be fully understood. Here we show that restricting the EMT of mammary epithelial cells by transcription factor Ovol2 is required for proper morphogenesis and regeneration. Deletion of Ovol2 blocks mammary ductal morphogenesis, depletes stem and progenitor cell reservoirs, and leads epithelial cells to undergo EMT in vivo to become nonepithelial cell types. Ovol2 directly represses myriad EMT inducers, and its absence switches response to TGF-β from growth arrest to EMT. Furthermore, forced expression of the repressor isoform of Ovol2 is able to reprogram metastatic breast cancer cells from a mesenchymal to an epithelial state. Our findings underscore the critical importance of exquisitely regulating epithelial plasticity in development and cancer.

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“…Terminal end buds (TEB), ducts, and empty fat pad were all collected from 6-week-old virgin BALB/c mice as described elsewhere (20).…”

Section: Methodsmentioning

confidence: 99%

Annexin A8 Is Up-Regulated During Mouse Mammary Gland Involution and Predicts Poor Survival in Breast Cancer

Stein

Price

Morris

et al. 2005

Clinical Cancer Research

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Purpose: Microarray studies have linked Annexin A8 RNA expression to a ''basal cell^like'' subset of breast cancers, including BRCA1-related cancers, that are characterized by cytokeratin 5 (CK5) and CK17 expression and show poor prognosis. We assessed Annexin A8's contribution to the overall prognosis and its expression in normal, benign, and cancerous tissue and addressed Annexin A8's physiologic role in the mammary gland. Experimental Design: Using microarrays and reverse transcription-PCR, the Annexin A8 expression was studied during mouse mammary gland development and in isolated mammary structures. Reverse transcription-PCR on cultured human luminal and basal cells, along with immunocytochemistry on normal and benign breast tissues, was used for cellular localization. Annexin A8's prognostic relevance and its coexpression with CK5 were assessed on tissue arrays of 1,631cases of invasive breast cancer. Coexpression was further evaluated on a small cohort of 14 BRCA1-related breast cancers. Results: Annexin A8 was up-regulated during mouse mammary gland involution and in pubertal ductal epithelium. Annexin A8 showed preferred expression in cultured basal cells but predominant luminal expression in normal human breast tissue in vivo. Hyperplasias and in situ carcinomas showed a strong staining of basal cells. Annexin A8 expression was significantly associated with grade (P < 0.0001), CK5 (P < 0.0001), and estrogen receptor status (P < 0.0001); 85.7% BRCA1-related breast tumors coexpressed Annexin A8 and CK5. Conclusion: Annexin A8 is involved in mouse mammary gland involution. In humans, it is a luminally expressed protein with basal expression in cell culture and in hyperplasia/ductal carcinoma in situ. Expression in invasive breast carcinomas has a significant effect on survival (P = 0.03) but is not independent of grade or CK5.

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Proteomic analysis of mouse mammary terminal end buds identifies axonal growth cone proteins

Cited by 9 publications

References 45 publications

Genetic Ablation of Caveolin-1 Drives Estrogen-Hypersensitivity and the Development of DCIS-Like Mammary Lesions

Genetic Ablation of Caveolin-1 Drives Estrogen-Hypersensitivity and the Development of DCIS-Like Mammary Lesions

Mammary Morphogenesis and Regeneration Require the Inhibition of EMT at Terminal End Buds by Ovol2 Transcriptional Repressor

Annexin A8 Is Up-Regulated During Mouse Mammary Gland Involution and Predicts Poor Survival in Breast Cancer

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