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Silencing the hsp25 Gene Eliminates Migration Capability of the Highly Metastatic Murine 4T1 Breast Adenocarcinoma CellBausero M.A.a, c · Bharti A.a · Page D.T.a · Perez K.D.a, b · Eng J.W.-L.a · Ordonez S.L.a · Asea E.E.a, b · Jantschitsch C.d · Kindas-Muegge I.e · Ciocca D.f · Asea A.a, b
aCenter for Molecular Stress Response, Boston University Medical Center and Boston University School of Medicine, Boston, Mass., bDivision of Investigative Pathology, Department of Pathology, Scott & White Clinic and Texas A&M University System Health Science Center College of Medicine, Temple, Tex., USA; cLaboratorio de Oncología Básica y Biología Molecular, Departamento de Bioquímica, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay; dDivision of Special and Environmental Dermatology, Department of Dermatology, University of Vienna, eInstitute of Cancer Research, Vienna, Austria; fInstitute of Experimental Medicine and Biology of Cuyo (IMBECU)-CONICET, Mendoza, Argentina Corresponding Author
Dr. Alexzander Asea, Division of Investigative Pathology
Scott & White Clinic and The Texas A&M University System Health Science Center College of Medicine, 2401 South 31st Street
Temple, TX 76508 (USA)
Tel. +1 254 743 0201, Fax +1 254 743 0247, E-Mail email@example.com
The 25-kDa heat shock protein (Hsp25) is associated with various malignancies and is expressed at high levels in biopsies as well as circulating in the serum of breast cancer patients. In this study, we used RNA interference technology to silence the hsp25 gene in 4T1 breast adenocarcinoma cells, known as a poorly immunogenic, highly metastatic cell line. We demonstrate that transfection of 4T1 cells with short interference RNA-Hsp25 dramatically inhibits proliferation as compared with control transfected cells. In addition, we show that 4T1 cells transfected with short interference RNA-Hsp25 abrogates tumor migration potential by a mechanism that is in part due to the repression of matrix metalloproteinase 9 expression and a concomitant upregulation of its antagonist, tissue inhibitor metalloproteinase 1. Taken together, these findings provide a model system for the study of metastatic potential of tumors and are suggestive of an earlier unrecognized role for Hsp25 in tumor migration.
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