ArrayExpress Uploader0mouseWild type NT2.5bone, liver, lungNT2.5 bone sub-line, 3rd passageboneNT2.5 bone sub-line, 6th passageboneNT2.5 liver sub-line, 1st passageliverNT2.5 liver sub-line, 3rd passageliver7330arrayexpress_sid6Breast cancer metastases develop in the bone more frequently than any other site, and are a common cause of morbidity in the form of bone...E-GEOD-47714/profile/8773/arrayexpressuploader25bonebreastbreast cancercancercellgenomehypercalcemialineliverlungnerveDec.12, 2014Falseosteotropism-in-breast-cancer-metastasisE-GEOD-47714_A-AFFY-45Osteotropism in breast cancer metastasisNov.12, 2014Breast cancer metastases develop in the bone more frequently than any other site, and are a common cause of morbidity in the form of bone pain, pathological fractures, nerve compression, and life-threatening hypercalcemia. Despite ongoing research efforts, the molecular and cellular mechanisms that regulate breast cancer cell homing to and colonization of the bone as well as resultant pathological bone alteration remain poorly understood. To identify key mediators promoting breast cancer metastasis to bone, we utilized an immunocompetent, syngeneic murine model of breast cancer metastasis employing the mammary tumor cell line NT2.5. Following intracardiac injection of NT2.5 cells in neu-N mice, metastases developed in the bone, liver, and lung, closely mimicking the anatomical distribution of metastases in breast cancer patients. Using an in vivo selection process, we established NT2.5 sub-lines demonstrating an enhanced ability to colonize the bone and liver. Genome-wide cDNA microarray analysis comparing gene expression between parental NT2.5 cells and established sub-lines was performed. Individual samples of RNA from parental NT2.5 cells, early passage (BO3 and LI1) sub-lines, and final passage (BO6 and LI3) sub-lines were compared using GeneChip® Mouse Genome 430 2.0 Arrayshttp://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-47714http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-47714/samples/