Gene expression patterns of a novel breast cancer cell line derived from a bone metastatic lesion of a breast cancer patient
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE55715 | GEO | 2021/01/31
REPOSITORIES: GEO
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Project description:As organ-specific models of breast cancer bone metastasis do not exist, we established a novel breast cancer line was established from the ER-/PR-/HER2- bone metastasis from a breast cancer patient. This cell line was characterized and compared to the primary tumour and/or normal mammary epithelial cells with regards to phenotypes (i.e. marker expression), gene expression and copy number variation.
2018-01-01 | GSE103896 | GEO
Project description:As organ-specific models of breast cancer bone metastasis do not exist, we established a novel breast cancer line was established from the ER-/PR-/HER2- bone metastasis from a breast cancer patient. This cell line was characterized and compared to the primary tumour and/or normal mammary epithelial cells with regards to phenotypes (i.e. marker expression), gene expression and copy number variation.
2018-02-23 | GSE103357 | GEO
Project description:Breast 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.
2013-06-07 | GSE47714 | GEO
Project description:Breast 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 Arrays
2013-06-07 | E-GEOD-47714 | biostudies-arrayexpress
Project description:Purpose: We sought to generate and characterize a novel cell line from a breast cancer bone metastasis in order to better study the progression of the disease.Methods: The cell line, P7731, was derived from a metastatic bone lesion of a breast cancer patient and assessed for marker expression. P7731 was analyzed for DNA copy number variation, somatic mutations and gene expression and compared to the primary tumor. Results: P7731 cells are negative for estrogen receptor alpha (ERα), progesterone receptor (PR) and HER2 (triple-negative), strongly express vimentin (100% of cells positive) and also express cytokeratins 8/18 and 19 but at lower frequencies. Flow cytometry indicates P7731 cells are predominantly CD44+/CD49f+/EpCAM-, consistent with a primitive, mesenchymal-like phenotype. The cell line is tumorigenic in immunocompromised mice. Exome sequencing identified a total of 45 and 76 somatic mutations in the primary tumor and cell line respectively, of which 32 were identified in both samples and included mutations in known driver genes PIK3CA, TP53 and ARID1A. P7731 retains the DNA copy number alterations present in the matching primary tumor. Homozygous deletions detected in the cell line and in the primary tumor were found in regions containing three known (CDKN2A, CDKN2B and CDKN1B) and 23 putative tumor suppressor genes. Cell line specific gene amplification coupled with mRNA expression analysis revealed genes and pathways with potential pro-metastatic functions.Conclusion: This novel human breast cancer-bone metastasis cell line will be a useful model to study aspects of breast cancer biology, particularly metastasis-related changes from breast to bone.
| EGAS00001002840 | EGA
Project description:Breast cancer research is hampered by difficulties in obtaining and studying primary human breast tissue, and by the lack of in vivo preclinical models that reflect patient tumor biology accurately. To overcome these limitations, we propagated a cohort of human breast tumors grown in the epithelium-free mammary fat pad of SCID/Beige and NOD/SCID/IL2γ-receptor null (NSG) mice, under a series of transplant conditions. Both models yielded stably transplantable xenografts at comparably high rates (~23% and ~19%, respectively). Of the conditions tested, xenograft take rate was highest in the presence of a low-dose estradiol pellet. Overall, 32 stably transplantable xenograft lines were established, representing unique 25 patients. Most tumors yielding xenografts were “triple-negative” (ER-PR-HER2+) (n=19). However, we established lines from three ER-PR-HER2+ tumors, one ER+PR-HER2-, one ER+PR+HER2- and one “triple-positive” (ER+PR+HER2+) tumor. Serially passaged xenografts show biological consistency with the tumor of origin, are phenotypic stability across multiple transplant generations at the histological, transcriptomic, proteomic, and genomic levels, and show comparable treatment responses. Xenografts representing 12 patients, including two ER+ lines, showed metastasis to the mouse lung. These models thus serve as a renewable, quality-controlled tissue resource for preclinical studies investigating treatment response and metastasis. The study was designed to determine how stable patient-derived xenografts are across multiple transplant generations in mice, and to determine how closely xenografts established with pre-treatment samples cluster with xenografts established with post-treatment samples. Overall, pre-treatment and post-treatment samples derived from the same patient cluster together, and multiple transplant generations of xenografts derived from an individual patient cluster together.
2013-05-30 | E-GEOD-46106 | biostudies-arrayexpress
Project description:Breast cancer research is hampered by difficulties in obtaining and studying primary human breast tissue, and by the lack of in vivo preclinical models that reflect patient tumor biology accurately. To overcome these limitations, we propagated a cohort of human breast tumors grown in the epithelium-free mammary fat pad of SCID/Beige and NOD/SCID/IL2γ-receptor null (NSG) mice, under a series of transplant conditions. Both models yielded stably transplantable xenografts at comparably high rates (~23% and ~19%, respectively). Of the conditions tested, xenograft take rate was highest in the presence of a low-dose estradiol pellet. Overall, 32 stably transplantable xenograft lines were established, representing unique 25 patients. Most tumors yielding xenografts were “triple-negative” (ER-PR-HER2+) (n=19). However, we established lines from three ER-PR-HER2+ tumors, one ER+PR-HER2-, one ER+PR+HER2- and one “triple-positive” (ER+PR+HER2+) tumor. Serially passaged xenografts show biological consistency with the tumor of origin, are phenotypic stability across multiple transplant generations at the histological, transcriptomic, proteomic, and genomic levels, and show comparable treatment responses. Xenografts representing 12 patients, including two ER+ lines, showed metastasis to the mouse lung. These models thus serve as a renewable, quality-controlled tissue resource for preclinical studies investigating treatment response and metastasis.
2013-05-30 | GSE46106 | GEO
Project description:Hormone receptor (HR) positive breast cancer, defined by expression of estrogen (ER) and/or progesterone (PR) receptor expression, is the most commonly diagnosed type of breast cancer. PR alters the transcriptional landscape to support tumor growth in concert with or independent of ER. Understanding the mechanisms regulating PR function are critical to developing new strategies to treat HR+ breast cancer. O-GlcNAc is a post-translational modification responsible for nutrient sensing that fine tunes protein function. We have previously reported O-GlcNAcylation on PR. Although PR is heavily post translationally modified, primarily through phosphorylation, specific sites of O-GlcNAcylation on PR, and how they regulate PR action, have not been investigated. Using established PR-expressing breast cancer cell lines, we mapped the sites of O-GlcNAcylation on PR. RNA-sequencing revealed site-specific O-GlcNAcylation of PR is critical for ligand-independent suppression of interferon signaling, a regulatory function of PR previously studied in our lab. Furthermore, O-GlcNAcylation of PR enhances PR-driven tumor growth in vivo. We have delineated one mechanism regulating PR function in breast cancer that impacts tumor growth, and provided additional insight into the mechanism through which PR attenuates interferon signaling.
2024-06-17 | MSV000095057 | MassIVE
Project description:Bone metastasis is an incurable complication of breast cancer. In advanced stages, patients with estrogen-positive tumors experience significantly higher incidence of bone metastasis compared to estrogen-negative patients. To investigate how estrogen-positive breast cancer cells communicate with bone microenvironmental cells, extracellular vesicles from bone metastatic MCF7BoM2 were purified and analyzed. We used GeneChip miRNA 4.1 Array to detail the miRNA expression in the extracellular vesicles from the bone metastatic MCF7BoM2 and its parental cell line MCF7, and identified the dysregulated miRNAs.
2021-06-04 | GSE176105 | GEO
Project description:The goal of this study was to evaluate genes that are differentially expressed in the bone stroma when breast cancer metastasis are present. We focused our attention on bone stroma cells to understand how the dissemination and growth of tumor cells can impact on the bone environment. Moreover, we aimed to identify potential targets to inhibit the cross talk between cancer cells and tumor microenvironment in bone metastasis. EO771 breast cancer cell line were engineered to express luciferase and GFP, and injected in C57BL/6 mice by the intracardiac route to obtain bone metastasis. Tumor growth was monitored in-vivo by bioluminescence for 2 weeks. Endothelial cells and osteoblasts were isolated from the long bones of tumor-bearing and tumor-free mice to identify genes differentially expressed.
2017-02-23 | GSE66205 | GEO