@article{3095239,
    title = "ERp29, an endoplasmic reticulum secretion factor is involved in the growth of breast tumor xenografts",
    author = "Mkrtchian, S. and Baryshev, M. and Sargsyan, E. and Chatzistamou, I. and Volakaki, A.-A. and Chaviaras, N. and Pafiti, A. and Triantafyllou, A. and Kiaris, H.",
    journal = "Molecular Carcinogenesis",
    year = "2008",
    volume = "47",
    number = "11",
    pages = "886-892",
    issn = "0899-1987, 1098-2744",
    doi = "10.1002/mc.20444",
    keywords = "cell protein;  endoplasmic reticulum protein 29;  small interfering RNA;  unclassified drug;  ERP29 protein, human;  Erp29 protein, rat;  heat shock protein, animal experiment;  animal model;  animal tissue;  article;  breast cancer;  breast epithelium;  breast tumor;  cancer cell;  cell differentiation;  cell proliferation;  controlled study;  female;  genetic transfection;  human;  human cell;  mammary gland;  mouse;  nonhuman;  priority journal;  protein expression;  tumor xenograft;  animal;  disease course;  endoplasmic reticulum;  gene expression regulation;  genetics;  metabolism;  nude mouse;  pathology;  rat;  secretion;  tumor cell line;  upregulation;  xenograft, Mus, Animals;  Breast Neoplasms;  Cell Line, Tumor;  Disease Progression;  Endoplasmic Reticulum;  Gene Expression Regulation, Neoplastic;  Heat-Shock Proteins;  Humans;  Mice;  Mice, Nude;  Rats;  Transplantation, Heterologous;  Up-Regulation",
    abstract = "Cancer cells are committed to an actively secretory state that facilitates communication with their microenvironment. We have addressed the role of ERp29, a novel endoplasmic reticulum secretion factor in mammary carcinogenesis using MCF-7 human breast cancer cells as a model. Xenografts originating from cells stably transfected with dominant-negative form of ERp29 were smaller and better differentiated than those derived from cells overexpressing wild-type ERp29. Similar effects were observed by siRNA-mediated ERp29 silencing in xenografts. However, unlike xenografts, the modulation of ERp29 in vitro did not affect the rate of cell proliferation. In addition, we have evaluated the expression of ERp29 in the resting and lactating mammary glands of mice as well as in the human primary breast tumors. About 25% of breast cancers and also lactating mammary glands were expressing ERp29 while the resting glands did not. Taken together these data suggest the active involvement of ERp29 in the malignant conversion of mammary epithelial cells. © 2008 Wiley-Liss, Inc."
}