Altered expression of microRNAs in bone metastasis compared with human prostate cancer
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus Rattus norvegicus Homo sapiens
PROVIDER: GSE26964 | GEO | 2011/01/31
SECONDARY ACCESSION(S): PRJNA136979
REPOSITORIES: GEO
Similar Datasets
Project description:The principal problem arising from prostate cancer (PCa) is its propensity to metastasize to bone. MicroRNAs (miRNAs) play a crucial role in many tumor metastases.The importance of miRNAs in bone metastasis of PCa has not been elucidated to date. We investigated whether the expression of certain miRNAs was associated with bone metastasis of PCa. We examined the miRNA expression profiles of 6 primary and 7 bone metastatic PCa samples by miRNA microarray analysis. Total RNA was taken from the specimens, low molecular weight RNA was seperate and labeled , and then hybridized to capitalbio V3.0 biochip representing about 924 microRNA.
2011-01-31 | E-GEOD-26964 | biostudies-arrayexpress
Project description:The propensity for prostate cancer to metastasize to bone led us and others to propose that bidirectional interaction between prostate cancer cells and bone are critical for the preferential metastasis of PCa to bone. We previous identified a secreted isoform of ErbB3 (p45-sErbB3) from the bone marrow supernatants of patients with prostate cancer and bone metastasis. Immunohistochemical analysis of p45-sErbB3 expression in human specimens showed that p45-sErbB3 was highly expressed in metastatic prostate cancer cells in bone. Here we show that p45-sErbB3 stimulates calvarial bone to secrete factors that increase the invasiveness of prostate cancer cells in Boyden chamber invasion assay. We used gene array analysis to identify p45-sErbB3 regulated osteoblast genes that may enhance the invasiveness of PC-3 cells and found that p45-sErbB3 stimulated the expression of osteonectin, biglycan, and type I collagen in mouse calvaria. We further showed that recombinant osteonectin increases the invasiveness of PC-3 cells and osteonectin neutralizing antibody blocked p45-sErbB3 mediated invasiveness. These results suggest that p45-sErbB3 enhances the invasiveness of PC-3 cells is due, at least in part, to the stimulation of the secretion of osteonectin from bone. Thus, p45-sErbB3 mediates the bi-directional interaction between PCa cells and bone through osteonectin. Sample 1: non-treated calvaria RNA, Group 1 Sample 2: sErbB3 (100ng/ml) treated calvaria RNA, Group 2 Array: GE-supper array MM026 (total 96 genes, with 10 housekeeping genes) (service from SuperArray Bioscience Corporation: http://www.superarray.com
2008-05-01 | E-GEOD-8001 | biostudies-arrayexpress
Project description:ER+ve and ER-ve breast cancers tend to show different patterns of metastasis, with ER+ve tumours having a propensity to metastasize to the bone while ER-ve tumours tend to induce visceral metastasis. Glycans can play an important role in metastasis through their interactions with glycan binding proteins. Moreover we, and others have also shown that expression of particular tumor-associated glycoforms of the mucin MUC1, allows it to interact with lectins of the immune system. We now have data showing differences in the level of expression of some glycosyltransferases in ER+ve and ER-ve of breast cancer suggesting the expression of different O-linked glycoforms.
2011-09-26 | GSE32394 | GEO
Project description:The propensity for prostate cancer to metastasize to bone led us and others to propose that bidirectional interaction between prostate cancer cells and bone are critical for the preferential metastasis of PCa to bone. We previous identified a secreted isoform of ErbB3 (p45-sErbB3) from the bone marrow supernatants of patients with prostate cancer and bone metastasis. Immunohistochemical analysis of p45-sErbB3 expression in human specimens showed that p45-sErbB3 was highly expressed in metastatic prostate cancer cells in bone. Here we show that p45-sErbB3 stimulates calvarial bone to secrete factors that increase the invasiveness of prostate cancer cells in Boyden chamber invasion assay. We used gene array analysis to identify p45-sErbB3 regulated osteoblast genes that may enhance the invasiveness of PC-3 cells and found that p45-sErbB3 stimulated the expression of osteonectin, biglycan, and type I collagen in mouse calvaria. We further showed that recombinant osteonectin increases the invasiveness of PC-3 cells and osteonectin neutralizing antibody blocked p45-sErbB3 mediated invasiveness. These results suggest that p45-sErbB3 enhances the invasiveness of PC-3 cells is due, at least in part, to the stimulation of the secretion of osteonectin from bone. Thus, p45-sErbB3 mediates the bi-directional interaction between PCa cells and bone through osteonectin. Keywords: Prostate cancer, bone metastasis, P45-sErbB3, osteonectin
2008-05-01 | GSE8001 | GEO
Project description:We found that RANKL, expressed by cancer cells or derived from exogenous sources, consistently induced human prostate, breast, kidney, lung and liver cancer cells to colonize or metastasize to bone in an animal model of cancer bone metastasis. RANK-mediated signaling established a premetastatic niche through a forward feedback loop by inducing RANKL and c-Met expression and downstream signaling via upregulation of master regulator transcription factors regulating EMT (Twist1, Slug, Zeb1, Zeb2), stem cells (Sox2, Myc, Oct3/4 and Nanog), neuroendocrine cells (Sox 9, HIF-1α and FoxA2) and osteomimicry (c-Myc/Max, Sox2, Sox9, HIF1α and Runx2). Abrogating RANK or its downstream signaling network, c-Myc/Max or c-Met, abolished PCa skeletal metastasis in mice. We observed that a small number of RANKL-expressing PCa cells can initiate bone and soft tissue metastases by recruiting non-tumorigenic or bystander PCa or host cells from the circulation or at metastatic sites to co-colonize bone. The recruited bystander PCa cells assume the phenotypes of RANKL-expressing PCa cells by expressing increased c-Met, phosphorylated c-Met and RANKL. RANKL expression at a single cell level in primary PCa tissues predicted disease-specific survival, reflecting the significant role of RANKL-RANK signaling in the development of lethal bone metastasis. Global gene expression analysis perturbed by RANKL in LNRANKL compared to LNNeo cells.
2014-02-06 | E-GEOD-48432 | biostudies-arrayexpress
Project description:We found that RANKL, expressed by cancer cells or derived from exogenous sources, consistently induced human prostate, breast, kidney, lung and liver cancer cells to colonize or metastasize to bone in an animal model of cancer bone metastasis. RANK-mediated signaling established a premetastatic niche through a forward feedback loop by inducing RANKL and c-Met expression and downstream signaling via upregulation of master regulator transcription factors regulating EMT (Twist1, Slug, Zeb1, Zeb2), stem cells (Sox2, Myc, Oct3/4 and Nanog), neuroendocrine cells (Sox 9, HIF-1α and FoxA2) and osteomimicry (c-Myc/Max, Sox2, Sox9, HIF1α and Runx2). Abrogating RANK or its downstream signaling network, c-Myc/Max or c-Met, abolished PCa skeletal metastasis in mice. We observed that a small number of RANKL-expressing PCa cells can initiate bone and soft tissue metastases by recruiting non-tumorigenic or bystander PCa or host cells from the circulation or at metastatic sites to co-colonize bone. The recruited bystander PCa cells assume the phenotypes of RANKL-expressing PCa cells by expressing increased c-Met, phosphorylated c-Met and RANKL. RANKL expression at a single cell level in primary PCa tissues predicted disease-specific survival, reflecting the significant role of RANKL-RANK signaling in the development of lethal bone metastasis.
2014-02-06 | GSE48432 | GEO
Project description:ER+ve and ER-ve breast cancers tend to show different patterns of metastasis, with ER+ve tumours having a propensity to metastasize to the bone while ER-ve tumours tend to induce visceral metastasis. Glycans can play an important role in metastasis through their interactions with glycan binding proteins. Moreover we, and others have also shown that expression of particular tumor-associated glycoforms of the mucin MUC1, allows it to interact with lectins of the immune system. We now have data showing differences in the level of expression of some glycosyltransferases in ER+ve and ER-ve of breast cancer suggesting the expression of different O-linked glycoforms. RNA will be isolated from ER+ve and ER-ve primary breast cancers supplied by the Guy’s and St Thomas’ Research Breast Tissue Bank. Tumor tissue will be macro-dissected from thick cryostat sections by visual comparison with a representative H&E section. We will verify the level of expression of ER and document the expression of ST3Gal-I and ST6GalNAc-II by RT-qPCR. We have already isolated RNA from a number of tumours and shown we can obtain RNA of good quality with a RNA integrity number, as measured with an Agilent Bioanalyser, of >4.5 Since there is likely to be variability among primary tumors, ideally we analyzed of 10 ER negative and 9 ER positive tumours.
2011-09-25 | E-GEOD-32394 | biostudies-arrayexpress
Project description:Prostate cancer (PCa) has a significant ability to disseminate and survive in the bone marrow (BM). Once there, disseminated tumor cells (DTCs) may lie dormant for years, but often eventually reactivate proliferative pathways, thus largely contributing to bone metastasis, disease progression, and relapse. Unfortunately, quiescent PCa cells are difficult to identify and target with treatment, in part because formerly identified relevant markers are intracellular and regulated by protein stability. We sought to address this problem by identifying a G0 marker that is expressed on the cell surface and therefore amenable to antibody binding for identification and therapeutic targeting. In doing so, we utilized stably transduced fluorescent markers for CDKN1B (p27) and CDT1 protein levels, which separate viable PCa cells into G0, G1, or combined S/G2/M populations (as described in PMID 34957090). We then performed FACS to collect G1 and G0 PC3 PCa cells, isolated membrane proteins, and subsequently used GC-MS proteomics to determine differences in protein abundance between G0 and G1. In total, 3,791 proteins were identified.
2023-03-03 | PXD037378 | Pride
Project description:Bone metastasis is the leading cause of prostate cancer (PCa) mortality, frequently marking the progression to castration-resistant PCa. In this study, we compared the molecular pathways enriched in a set of bone metastasis from breast and prostate cancer from snap-frozen tissue. To further model PCa drug resistance mechanisms, we used two patient-derived xenografts (PDX) models of bone-metastatic PCa, BM18 and LAPC9.
| EGAS00001004431 | EGA
Project description:Purpose: The goals of this study are to compare the serum extracellular vesicle (EV) delivered miRNA levels of patients with bone-metastatic prostate cancer (PCa), non-bone -metastatic PCa and benign prostatic hyperplasia (BPH), and to identify EV-delivered microRNAs in patient’s serum as indicators for bone-metastatic PCa. Methods:Serum extracellular vesicle delivered miRNA profiles of patients with bone-metastatic PCa or non-bone -metastatic PCa or BPH were generated by miRNA chip array, using Agilent-070156 Human_miRNA_V21.0_Microarray plateform. Results: Differential analysis showed the expressions of 27 EV delivered miRNAs were significantly different between serum of patients with bone-metastatic PCa and non-bone-metastatic PCa with a p value <0.05. the expressions of 5 EV delivered miRNAs were confirmed with qRT–PCR. Conclusions: Serum EV-delivered miR-181a-5p is a promising diagnostic biomarker for bone-metastatic PCa.
2020-01-31 | GSE134266 | GEO