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  1 / 2699 MEDLINE  
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PMID:28079891
Autor:Mao X; Li P; Wang Y; Liang Z; Liu J; Li J; Jiang Y; Bao G; Li L; Zhu B; Ren Y; Zhao X; Zhang J; Liu Y; Yang J; Liu P
Dirección:Center for Translational Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.
Título:CRB3 regulates contact inhibition by activating the Hippo pathway in mammary epithelial cells.
Fuente:Cell Death Dis; 8(1):e2546, 2017 Jan 12.
ISSN:2041-4889
País de publicación:England
Idioma:eng
Resumen:The loss of contact inhibition is a hallmark of cancer cells. The Hippo pathway has recently been shown to be an important regulator of contact inhibition, and the cell apical polarity determinant protein CRB3 has been suggested to be involved in Hippo signalling. However, whether CRB3 regulates contact inhibition in mammary cells remains unclear, and the underlying mechanisms have not been elucidated. As shown in the present study, CRB3 decreases cell proliferation, promotes apoptosis, and enhances the formation of tight and adherens junctions. Furthermore, we report for the first time that CRB3 acts as an upstream regulator of the Hippo pathway to regulate contact inhibition by recruiting other Hippo molecules, such as Kibra and/or FRMD6, in mammary epithelial cells. In addition, CRB3 inhibits tumour growth in vivo. Collectively, the present study increases our understanding of the Hippo pathway and provides an important theoretical basis for exploring new avenues for breast cancer treatment.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:0 (CRB3 protein, human); 0 (Cytoskeletal Proteins); 0 (FRMD6 protein, human); 0 (Intracellular Signaling Peptides and Proteins); 0 (Membrane Glycoproteins); 0 (Membrane Proteins); 0 (Phosphoproteins); 0 (WWC1 protein, human); EC 2.7.11.1 (Hippo protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)


  2 / 2699 MEDLINE  
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PMID:28379851
Autor:Ghani MU; Wong MD; Wu D; Zheng B; Fajardo LL; Yan A; Fuh J; Wu X; Liu H
Dirección:Center for Biomedical Engineering and School of Electrical and Computer Engineering, University of Oklahoma, Norman, OK 73019, United States of America.
Título:Detectability comparison between a high energy x-ray phase sensitive and mammography systems in imaging phantoms with varying glandular-adipose ratios.
Fuente:Phys Med Biol; 62(9):3523-3538, 2017 May 07.
ISSN:1361-6560
País de publicación:England
Idioma:eng
Resumen:The objective of this study was to demonstrate the potential benefits of using high energy x-rays in comparison with the conventional mammography imaging systems for phase sensitive imaging of breast tissues with varying glandular-adipose ratios. This study employed two modular phantoms simulating the glandular (G) and adipose (A) breast tissue composition in 50 G-50 A and 70 G-30 A percentage densities. Each phantom had a thickness of 5 cm with a contrast detail test pattern embedded in the middle. For both phantoms, the phase contrast images were acquired using a micro-focus x-ray source operated at 120 kVp and 4.5 mAs, with a magnification factor (M) of 2.5 and a detector with a 50 µm pixel pitch. The mean glandular dose delivered to the 50 G-50 A and 70 G-30 A phantom sets were 1.33 and 1.3 mGy, respectively. A phase retrieval algorithm based on the phase attenuation duality that required only a single phase contrast image was applied. Conventional low energy mammography images were acquired using GE Senographe DS and Hologic Selenia systems utilizing their automatic exposure control (AEC) settings. In addition, the automatic contrast mode (CNT) was also used for the acquisition with the GE system. The AEC mode applied higher dose settings for the 70 G-30 A phantom set. As compared to the phase contrast images, the dose levels for the AEC mode acquired images were similar while the dose levels for the CNT mode were almost double. The observer study, contrast-to-noise ratio and figure of merit comparisons indicated a large improvement with the phase retrieved images in comparison to the AEC mode images acquired with the clinical systems for both density levels. As the glandular composition increased, the detectability of smaller discs decreased with the clinical systems, particularly with the GE system, even at higher dose settings. As compared to the CNT mode (double dose) images, the observer study also indicated that the phase retrieved images provided similar or improved detection for all disc sizes except for the disk diameters of 2 mm and 1 mm for the 50 G-50 A phantom and 3 mm and 0.5 mm for the 70 G-30 A phantom. This study demonstrated the potential of utilizing a high energy phase sensitive x-ray imaging system to improve lesion detection and reduce radiation dose when imaging breast tissues with varying glandular compositions.
Tipo de publicación:COMPARATIVE STUDY; JOURNAL ARTICLE


  3 / 2699 MEDLINE  
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PMID:29022488
Autor:Joshi PS; Modur V; Cheng J; Robinson K; Rao K
Dirección:1 Department of Medical Microbiology, Immunology and Cell Biology, Southern Illinois University School of Medicine, Springfield, IL, USA.
Título:Characterization of immortalized human mammary epithelial cell line HMEC 2.6.
Fuente:Tumour Biol; 39(10):1010428317724283, 2017 Oct.
ISSN:1423-0380
País de publicación:United States
Idioma:eng
Resumen:Primary human mammary epithelial cells have a limited life span which makes it difficult to study them in vitro for most purposes. To overcome this problem, we have developed a cell line that was immortalized using defined genetic elements, and we have characterized this immortalized non-tumorigenic human mammary epithelial cell line to establish it as a potential model system. human mammary epithelial cells were obtained from a healthy individual undergoing reduction mammoplasty at SIU School of Medicine. The cells were transduced with CDK4R24C followed by transduction with human telomerase reverse transcriptase. Post all manipulation, the cells displayed a normal cell cycle phase distribution and were near diploid in nature, which was confirmed by flow cytometry and karyotyping. In vitro studies showed that the cells were anchorage dependent and were non-invasive in nature. The cell line expressed basal epithelial markers such as cytokeratin 7, CD10, and p63 and was negative for the expression of estrogen receptor and progesterone receptor. Upon G-band karyotyping, the cell line displayed the presence of a few cytogenic abnormalities, including trisomy 20 and trisomy 7, which are also commonly present in other immortalized mammary cell lines. Furthermore, the benign nature of these cells was confirmed by multiple in vitro and in vivo experiments. Therefore, we think that this cell line could serve as a good model to understand the molecular mechanisms involved in the development and progression of breast cancer and to also assess the effect of novel therapeutics on human mammary epithelial cells.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:EC 2.7.11.22 (CDK4 protein, human); EC 2.7.11.22 (Cyclin-Dependent Kinase 4); EC 2.7.7.49 (TERT protein, human); EC 2.7.7.49 (Telomerase)


  4 / 2699 MEDLINE  
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PMID:28859163
Autor:Che W; Bao Y; Tang F
Dirección:Huashan Hospital of Fudan University, Shanghai, China.
Título:Down-regulation of C35 decreased the cell viability and migration of breast ductal carcinoma cells.
Fuente:PLoS One; 12(8):e0183941, 2017.
ISSN:1932-6203
País de publicación:United States
Idioma:eng
Resumen:BACKGROUND: Resistance to human epidermal growth factor receptor-2 (HER2)-targeted therapies is common, and results in treatment failure and new tumor progression. C35 is over-expressed in many invasive breast cancer endogenously, and functions as an oncogene in breast cancer cell lines. METHODS: The current study aims to investigate effects of C35 on cell viability and migration of HER2-positive breast tumor cells and explore possible mechanisms. The protein expression of C35 in BT-474 breast ductal carcinoma cells was interfered by siRNAs. MTT assay was utilized to detect the viability of BT474 breast ductal carcinoma cells after transfection. The migration of BT474 breast ductal carcinoma cells was examined by cell wound scratch assay. RESULTS: In addition, the protein expression of C35, HER2, AKT and p-AKT in breast ductal carcinoma cells were detected by Western Blot. The protein expression of C35 was weaker in siRNA1 and siRNA2 groups compared with the control group. The relative expression ratio of C35 to ß-actin decreased significantly in siRNA2 and siRNA1 groups. When C35 expression was interfered by siRNA1 and siRNA2 for 48 h, the viability of BT474 breast ductal carcinoma cells decreased compared with the control group. In addition, the migration of breast ductal carcinoma cells decreased when C35 expression was interfered by siRNA1 for 24 h, and interfered by siRNA1 and siRNA2 for 48 h.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:0 (Intracellular Signaling Peptides and Proteins); 0 (MIEN1 protein, human); 0 (Neoplasm Proteins); 0 (RNA, Small Interfering); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Receptor, ErbB-2); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)


  5 / 2699 MEDLINE  
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PMID:28800960
Autor:Chean J; Chen CJ; Shively JE
Dirección:Department of Molecular Immunology, Beckman Research Institute of City of Hope, 1450 E. Duarte Road, Duarte, CA 91010, USA.
Título:ETS transcription factor ELF5 induces lumen formation in a 3D model of mammary morphogenesis and its expression is inhibited by Jak2 inhibitor TG101348.
Fuente:Exp Cell Res; 359(1):62-75, 2017 Oct 01.
ISSN:1090-2422
País de publicación:United States
Idioma:eng
Resumen:The loss of expression of a single gene can revert normal tissue to a malignant phenotype. For example, while normal breast has high lumenal expression of CEACAM1, the majority of breast cancers exhibit the early loss of this gene with the concurrent loss of their lumenal phenotype. MCF7 cells that lack CEACAM1 expression and fail to form lumena in 3D culture, regain the normal phenotype when transfected with CEACAM1. In order to probe the mechanism of this gain of function, we treated these cells with the clinically relevant Jak2 inhibitor TG101348 (TG), expecting that disruption of the prolactin receptor signaling pathway would interfere with the positive effects of transfection of MCF7 cells with CEACAM1. Indeed, lumen formation was inhibited, resulting in the down regulation of a set of genes, likely involved in the complex process of lumen formation. As expected, inhibition of the expression of many of these genes also inhibited lumen formation, confirming their involvement in a single pathway. Among the genes identified by the inhibition assay, ETS transcription factor ELF5 stood out, since it has been identified as a master regulator of mammary morphogenesis, and is associated with prolactin receptor signaling. When ELF5 was transfected into the parental MCF7 cells that lack CEACAM1, lumen formation was restored, indicating that ELF5 can replace CEACAM1 in this model system of lumenogenesis. We conclude that the event(s) that led to the loss of expression of CEACAM1 is epistatic in that multiple genes associated with a critical pathway were affected, but that restoration of the normal phenotype can be achieved with reactivation of certain genes at various nodal points in tissue morphogenesis.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:0 (ELF5 protein, human); 0 (Neoplasm Proteins); 0 (Protein Kinase Inhibitors); 0 (Proto-Oncogene Proteins c-ets); 0 (Pyrrolidines); 0 (RNA, Antisense); 0 (RNA, Messenger); 0 (SOCS2 protein, human); 0 (STAT5 Transcription Factor); 0 (STAT5A protein, human); 0 (Sulfonamides); 0 (Suppressor of Cytokine Signaling Proteins); 0 (TG101348); 0 (Tumor Suppressor Proteins); EC 2.7.10.2 (Janus Kinase 2)


  6 / 2699 MEDLINE  
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PMID:28938116
Autor:Hannezo E; Scheele CLGJ; Moad M; Drogo N; Heer R; Sampogna RV; van Rheenen J; Simons BD
Dirección:Cavendish Laboratory, Department of Physics, University of Cambridge, Cambridge CB3 0HE, UK; The Wellcome Trust/Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, UK; The Wellcome Trust/Medical Research Council Stem Cell Institute, University of Cambridge, Cambridge CB2
Título:A Unifying Theory of Branching Morphogenesis.
Fuente:Cell; 171(1):242-255.e27, 2017 Sep 21.
ISSN:1097-4172
País de publicación:United States
Idioma:eng
Resumen:The morphogenesis of branched organs remains a subject of abiding interest. Although much is known about the underlying signaling pathways, it remains unclear how macroscopic features of branched organs, including their size, network topology, and spatial patterning, are encoded. Here, we show that, in mouse mammary gland, kidney, and human prostate, these features can be explained quantitatively within a single unifying framework of branching and annihilating random walks. Based on quantitative analyses of large-scale organ reconstructions and proliferation kinetics measurements, we propose that morphogenesis follows from the proliferative activity of equipotent tips that stochastically branch and randomly explore their environment but compete neutrally for space, becoming proliferatively inactive when in proximity with neighboring ducts. These results show that complex branched epithelial structures develop as a self-organized process, reliant upon a strikingly simple but generic rule, without recourse to a rigid and deterministic sequence of genetically programmed events.
Tipo de publicación:JOURNAL ARTICLE


  7 / 2699 MEDLINE  
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PMID:27773611
Autor:Xiong N; Li S; Tang K; Bai H; Peng Y; Yang H; Wu C; Liu Y
Dirección:Department of Biophysics, School of Life Science and Technology, University of Electronic Science and Technology of China, Chengdu 610054, Sichuan, PR China.
Título:Involvement of caveolin-1 in low shear stress-induced breast cancer cell motility and adhesion: Roles of FAK/Src and ROCK/p-MLC pathways.
Fuente:Biochim Biophys Acta; 1864(1):12-22, 2017 01.
ISSN:0006-3002
País de publicación:Netherlands
Idioma:eng
Resumen:Tumor cells translocating to distant sites are subjected to hemodynamic shear forces during their passage in the blood vessels. Low shear stress (LSS) plays a critical role in the regulation of various aspects of tumor cells functions, including motility and adhesion. Beyond its structural role, caveolin-1 (Cav-1), the important component of caveolae, represents a modulator of several cancer-associated functions as tumor progression and metastasis. However, the role of Cav-1 in regulating tumor cells response to shear stress remains poorly explored. Here, we characterized the role of LSS and Cav-1 in mediating cell motility and adhesion on human breast carcinoma MDA-MB-231 cells. We first showed that LSS exposure promoted cell polarity and focal adhesion (FA) dynamics, thus indicating elevated cell migration. Silencing of Cav-1 leaded to a significantly lower formation of stress fibers. However, LSS exposure was able to rescue it via the alteration of actin-associated proteins expression, including ROCK, p-MLC, cofilin and filamin A. Time-lapse migration assay indicated that Cav-1 expression fostered MDA-MB-231 cells motility and LSS triggered cells to rapidly generate new lamellipodia. Furthermore, Cav-1 and LSS significantly influenced cell adhesion. Taken together, our findings provide insights into mechanisms underlying LSS triggered events mediated by downstream Cav-1, including FAK/Src and ROCK/p-MLC pathways, involved in the reorganization of the cytoskeleton, cell motility, FA dynamics and breast cancer cell adhesion.
Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Nombre de substancia:0 (CAV1 protein, human); 0 (CFL1 protein, human); 0 (Caveolin 1); 0 (Cofilin 1); 0 (Filamins); 0 (MLC1 protein, human); 0 (Membrane Proteins); 0 (RNA, Small Interfering); EC 2.7.10.2 (Focal Adhesion Kinase 1); EC 2.7.10.2 (PTK2 protein, human); EC 2.7.10.2 (src-Family Kinases); EC 2.7.11.1 (ROCK1 protein, human); EC 2.7.11.1 (rho-Associated Kinases)


  8 / 2699 MEDLINE  
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PMID:28118035
Autor:El Khoury M; Sanchez LM; Lalonde L; Trop I; David J; Mesurolle B
Dirección:1 Department of Radiology, Breast Centre, Centre Hospitalier Universitaire de Montréal, Montreal, QC, Canada.
Título:Is the outcome at surgery different when flat epithelial atypia and lobular neoplasia are found in association at biopsy?
Fuente:Br J Radiol; 90(1072):20160750, 2017 Apr.
ISSN:1748-880X
País de publicación:England
Idioma:eng
Resumen:OBJECTIVE: To assess the impact on the final outcome at surgery of flat epithelial atypia (FEA) when found concomitantly with lobular neoplasia (LN) in biopsy specimens compared with pure biopsy-proven FEA. METHODS: The approval from the institutional review board of the CHUM (Centre Hospitalier Universitaire de Montréal) was obtained. A retrospective review of our database between 2009 and 2013 identified 81 females (mean age 54 years, range 38-90 years) with 81 FEA biopsy-proven lesions. These were pure or associated with LN only in 59/81 (73%) and 22/81 (27%) cases, respectively. Overall, 57/81 (70%) patients underwent surgery and 24/81 (30%) patients underwent mammographic surveillance with a mean follow-up of 36 months. RESULTS: FEA presented more often as microcalcifications in 68/81 (84%) patients and were mostly amorphous in 49/68 (72%). After excluding radio pathologically discordant cases, pure FEA proved to be malignant at surgery in 1/41 (2%; 95% confidence interval 0.06-12.9). There was no statistically significant difference in the upgrade to malignancy whether FEA lesions were pure or associated to LN at biopsy (p = 0.4245); however, when paired in biopsy specimens, these lesions were more frequently associated with atypical ductal hyperplasia (ADH) at surgery than with pure FEA (p = 0.012). CONCLUSION: Our results show a 2% upgrade rate to malignancy of pure FEA lesions. When FEA is found in association with LN at biopsy, surgical excision yields more frequently ADH than pure FEA thus warranting close surveillance or even surgical excision. Advances in knowledge: The association of LN with FEA at biopsy was more frequently associated with ADH at surgery than with pure FEA. If a biopsy-proven FEA lesion is deemed concordant with the imaging finding, when paired with LN at biopsy, careful surveillance or even surgical excision is suggested.
Tipo de publicación:JOURNAL ARTICLE


  9 / 2699 MEDLINE  
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PMID:27974362
Autor:Peuhu E; Kaukonen R; Lerche M; Saari M; Guzmán C; Rantakari P; De Franceschi N; Wärri A; Georgiadou M; Jacquemet G; Mattila E; Virtakoivu R; Liu Y; Attieh Y; Silva KA; Betz T; Sundberg JP; Salmi M; Deugnier MA; Eliceiri KW; Ivaska J
Dirección:Centre for Biotechnology, University of Turku, Turku, Finland emilia.peuhu@utu.fi johanna.ivaska@utu.fi.
Título:SHARPIN regulates collagen architecture and ductal outgrowth in the developing mouse mammary gland.
Fuente:EMBO J; 36(2):165-182, 2017 Jan 17.
ISSN:1460-2075
País de publicación:England
Idioma:eng
Resumen:SHARPIN is a widely expressed multifunctional protein implicated in cancer, inflammation, linear ubiquitination and integrin activity inhibition; however, its contribution to epithelial homeostasis remains poorly understood. Here, we examined the role of SHARPIN in mammary gland development, a process strongly regulated by epithelial-stromal interactions. Mice lacking SHARPIN expression in all cells (Sharpin ), and mice with a stromal (S100a4-Cre) deletion of Sharpin, have reduced mammary ductal outgrowth during puberty. In contrast, Sharpin mammary epithelial cells transplanted in vivo into wild-type stroma, fully repopulate the mammary gland fat pad, undergo unperturbed ductal outgrowth and terminal differentiation. Thus, SHARPIN is required in mammary gland stroma during development. Accordingly, stroma adjacent to invading mammary ducts of Sharpin mice displayed reduced collagen arrangement and extracellular matrix (ECM) stiffness. Moreover, Sharpin mammary gland stromal fibroblasts demonstrated defects in collagen fibre assembly, collagen contraction and degradation in vitro Together, these data imply that SHARPIN regulates the normal invasive mammary gland branching morphogenesis in an epithelial cell extrinsic manner by controlling the organisation of the stromal ECM.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:0 (Carrier Proteins); 0 (Sipl1 protein, mouse); 9007-34-5 (Collagen)


  10 / 2699 MEDLINE  
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PMID:28436180
Autor:Isobe N
Dirección:Graduate School of Biosphere Science, Hiroshima University, Higashi-Hiroshima, Japan.
Título:Control mechanisms for producing antimicrobial factors in ruminant mammary gland.
Fuente:Anim Sci J; 88(7):937-943, 2017 Jul.
ISSN:1740-0929
País de publicación:Australia
Idioma:eng
Resumen:Mastitis, a symptom of inflammation in mammary tissue by infection with various kinds of bacteria, causes huge economic losses in the milk industry. One of the popular methods for treatment of mastitis is antibiotics, although this prohibits milk shipping and sometimes causes resistant microbes. Therefore, a new strategy to treat mastitis without antibiotics is eagerly required around the world. Antimicrobial factors belong to innate immunity and can start their function extremely early after bacterial stimulation. These factors have antimicrobial activity for a broad spectrum of bacteria. Elucidation of causal mechanisms and functions of antimicrobial factors in the mammary gland is thought to result in suitable methods for prevention and treatment of mastitis. Therefore, this review introduces traits of some antimicrobial factors and the mechanisms for expressing, producing and secreting them in the mammary gland. For antimicrobial factors, lingual antimicrobial peptide (LAP), S100A7, cathelicidin and lactoferrin are controlled in different sites and different time courses, suggesting that antimicrobial factors play different roles for local defense against bacterial infection in the mammary gland. These findings will contribute to the development of prevention and treatment methods for mastitis.
Tipo de publicación:JOURNAL ARTICLE; REVIEW
Nombre de substancia:0 (Antimicrobial Cationic Peptides); 0 (S100 Proteins); 0 (S100A7 protein, human); 0 (beta-Defensins); 0 (lingual antimicrobial peptide); 143108-26-3 (CAP18 lipopolysaccharide-binding protein); EC 3.4.21.- (Lactoferrin)



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