Expression data from LNCaP cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE78196 | GEO | 2016/02/23
SECONDARY ACCESSION(S): PRJNA312902
REPOSITORIES: GEO
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Project description:Prostate Cancer Stem Cells (CSCs) are considered one of the main reasons the tumor recurrence after chemotherapy. Here we employed a chemoresistant xenograft prostate cancer model in NOD/SCID mice and found CD54 is a reliable new marker for prostate CSCs. Gene expression profile were utilized to analyze stemness-related genes in cancer stem cells. 12 Male NOD/SCID mice were obtained from the Animal Center of the Chinese Academy of Medical Science (Beijing, China). For xenograft generation, 1Ã106 LNCaP cells were subcutaneously injected into the backs of NOD/SCID mice (n=24). When tumors reached a diameter of 5 mm after 3 d, mice were randomly divided into two groups without castration (12 per group). Mice in the treatment group were administered with cisplatin at a dose of 5 mg/kg every 3 d for 30 d. Mice in the control group were treated with vehicle PBS. Tumors were taken out for microarray assay after 30 d.
2016-02-23 | E-GEOD-78196 | biostudies-arrayexpress
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Project description:LNCAP xenograft prostate cancer progression model in NOD-SCID mice
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Project description:Cancer stem cells (CSCs) drive prostate cancer (PCa) progression and metastasis. These cells exhibit remarkable self-renewal, chemoresistant and invasive potentials, and are thought to participate in the changes in cellular architecture that lead to epithelial-to-mesenchymal transition (EMT). Conventional therapies fail to eliminate CSCs, which results in tumor recurrence and progression to castration resistant PCa (CRPC). Recent evidence suggests that castration itself can induce EMT, which could potentiate the âstemnessâ and number of CSCs within the tumor. Hence, there is an urgent need for EMT- and CSC-targeted therapies that could prevent progression to CRPC. 22Rv1, DU145, LNCaP, and PC3 cells were grown under sphere-forming conditions standardized in our lab. We have previously demonstrated that these enriched PCa cell lines exhibit phenotypic characteristics associated with CSCs in vivo. Over-expression of the stem-associated CD133 biomarker was determined via flow cytometric analysis. Total RNA was isolated from CD133+ prostasphere-derived cells. Gene expression profiling was carried out using the nCounter NanoString system and three different CodeSets associated with cancer or stem cells. Functional annotation was performed using the over-representation analysis tool from ConsensusPathDB. Functional annotation analysis of upregulated transcripts suggests that prostasphere-derived cells undergo a transcriptional reprogramming that triggers a major phenotypic shift. These changes are similar to the mesenchymal shift associated with EMT that drives PCa progression to CRPC. Each cell line exhibited distinct expression profiles that are presented and analyzed individually. Furthermore, our analysis revealed over-represented pathways that were common to all cell lines, which are related to the MAPK/ERK, PI3K/AKT, Notch, and Wnt stem cell fate signaling networks. Transcriptional analysis of induced CSCs not only offers insight into their underlying pathophysiology, but can also be used as a platform for the discovery of therapeutic targets for CSC-specific intervention. In this contribution, we present a flexible in vitro platform for the identification of functionally relevant therapeutic targets, using cell samples with low numbers of malignant stem/progenitors that were enriched in vitro. This approach represents a novel and effective strategy that can be used in the development of therapeutic strategies, which could ultimately be tailored to the biology of individual patients. 22Rv1, DU145, LNCaP and PC3 prostasphere cultures were sampled on Day 4 (P 2), Day 8 (P 3) and Day 12 (P 4), and compared relative to parental monolayers on Day 0 of culture (P 1). Three independent measurements were carried out for monolayers at Day 0 using the CancerReference Kit. Day 12 prostaspheres were enzymatically dissociated and sorted via MACS using the Anti-CD133/2 (293C3)-PE Antibody (Miltenyi) into CD133+ and CD133- fractions. Total RNA was extracted from CD133+ cells and were analyzed using the nCounter GX Cancer Reference kit, the Stem Cell panel and the custom made ITESM CodeSet (14 genes associated with prostate cancer) from NanoString Technologies. This series contains data for the Stem Cell panel.
2016-02-06 | E-GEOD-77613 | biostudies-arrayexpress
Project description:Glioblastoma multiforme (GBM) is a lethal malignancy whose clinical intransigence has been linked to extensive intra-clonal genetic and phenotypic diversity and therapeutic resistance of cancer stem cells (CSCs). This interpretation embodies an implicit assumption that CSCs are themselves genetically diverse. To test this, we screened neurosphere cultures by SNP arrays to identify copy number alterations (CNA) (minimum of three) that could be visualised in single cells by multi-colour FISH. Interrogation of neurosphere-derived cells (from four patients) and cells derived from secondary transplants of these same cells in Nod/Scid mice allowed us to infer clonal phylogenic architecture and the likely derivation of functional CSCs. This proof-of-principle experiment revealed that more than one sub-clone (but not all) in each GBM had functionally defined, genetically distinct stem cells.
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Project description:Cancer stem cells (CSCs) drive prostate cancer (PCa) progression and metastasis. These cells exhibit remarkable self-renewal, chemoresistant and invasive potentials, and are thought to participate in the changes in cellular architecture that lead to epithelial-to-mesenchymal transition (EMT). Conventional therapies fail to eliminate CSCs, which results in tumor recurrence and progression to castration resistant PCa (CRPC). Recent evidence suggests that castration itself can induce EMT, which could potentiate the â??stemnessâ?? and number of CSCs within the tumor. Hence, there is an urgent need for EMT- and CSC-targeted therapies that could prevent progression to CRPC. 22Rv1, DU145, LNCaP, and PC3 cells were grown under sphere-forming conditions standardized in our lab. We have previously demonstrated that these enriched PCa cell lines exhibit phenotypic characteristics associated with CSCs in vivo. Over-expression of the stem-associated CD133 biomarker was determined via flow cytometric analysis. Total RNA was isolated from CD133+ prostasphere-derived cells. Gene expression profiling was carried out using the nCounter NanoString system and three different CodeSets associated with cancer or stem cells. Functional annotation was performed using the over-representation analysis tool from ConsensusPathDB. Functional annotation analysis of upregulated transcripts suggests that prostasphere-derived cells undergo a transcriptional reprogramming that triggers a major phenotypic shift. These changes are similar to the mesenchymal shift associated with EMT that drives PCa progression to CRPC. Each cell line exhibited distinct expression profiles that are presented and analyzed individually. Furthermore, our analysis revealed over-represented pathways that were common to all cell lines, which are related to the MAPK/ERK, PI3K/AKT, Notch, and Wnt stem cell fate signaling networks. Transcriptional analysis of induced CSCs not only offers insight into their underlying pathophysiology, but can also be used as a platform for the discovery of therapeutic targets for CSC-specific intervention. In this contribution, we present a flexible in vitro platform for the identification of functionally relevant therapeutic targets, using cell samples with low numbers of malignant stem/progenitors that were enriched in vitro. This approach represents a novel and effective strategy that can be used in the development of therapeutic strategies, which could ultimately be tailored to the biology of individual patients. 22Rv1, DU145, LNCaP and PC3 prostasphere cultures were sampled on Day 4 (P 2), Day 8 (P 3) and Day 12 (P 4), and compared relative to parental monolayers on Day 0 of culture (P 1). Three independent measurements were carried out for monolayers at Day 0 using the CancerReference Kit. Day 12 prostaspheres were enzymatically dissociated and sorted via MACS using the Anti-CD133/2 (293C3)-PE Antibody (Miltenyi) into CD133+ and CD133- fractions. Total RNA was extracted from CD133+ cells and analyzed using the nCounter GX Cancer Reference kit, the Stem Cell panel and the custom made ITESM CodeSet from NanoString Technologies. This series contains the Cancer Reference kit data.
2016-02-06 | E-GEOD-77612 | biostudies-arrayexpress
Project description:Cancer stem cells (CSCs) drive prostate cancer (PCa) progression and metastasis. These cells exhibit remarkable self-renewal, chemoresistant and invasive potentials, and are thought to participate in the changes in cellular architecture that lead to epithelial-to-mesenchymal transition (EMT). Conventional therapies fail to eliminate CSCs, which results in tumor recurrence and progression to castration resistant PCa (CRPC). Recent evidence suggests that castration itself can induce EMT, which could potentiate the âstemnessâ and number of CSCs within the tumor. Hence, there is an urgent need for EMT- and CSC-targeted therapies that could prevent progression to CRPC. 22Rv1, DU145, LNCaP, and PC3 cells were grown under sphere-forming conditions standardized in our lab. We have previously demonstrated that these enriched PCa cell lines exhibit phenotypic characteristics associated with CSCs in vivo. Over-expression of the stem-associated CD133 biomarker was determined via flow cytometric analysis. Total RNA was isolated from CD133+ prostasphere-derived cells. Gene expression profiling was carried out using the nCounter NanoString system and three different CodeSets associated with cancer or stem cells. Functional annotation was performed using the over-representation analysis tool from ConsensusPathDB. Functional annotation analysis of upregulated transcripts suggests that prostasphere-derived cells undergo a transcriptional reprogramming that triggers a major phenotypic shift. These changes are similar to the mesenchymal shift associated with EMT that drives PCa progression to CRPC. Each cell line exhibited distinct expression profiles that are presented and analyzed individually. Furthermore, our analysis revealed over-represented pathways that were common to all cell lines, which are related to the MAPK/ERK, PI3K/AKT, Notch, and Wnt stem cell fate signaling networks. Transcriptional analysis of induced CSCs not only offers insight into their underlying pathophysiology, but can also be used as a platform for the discovery of therapeutic targets for CSC-specific intervention. In this contribution, we present a flexible in vitro platform for the identification of functionally relevant therapeutic targets, using cell samples with low numbers of malignant stem/progenitors that were enriched in vitro. This approach represents a novel and effective strategy that can be used in the development of therapeutic strategies, which could ultimately be tailored to the biology of individual patients. 22Rv1, DU145, LNCaP and PC3 prostasphere cultures were sampled on Day 4 (P 2), Day 8 (P 3) and Day 12 (P 4), and compared relative to parental monolayers on Day 0 of culture (P 1). Three independent measurements were carried out for monolayers at Day 0 using the CancerReference Kit. were sampled Day 12 prostaspheres were enzymatically dissociated and sorted via MACS using the Anti-CD133/2 (293C3)-PE Antibody (Miltenyi) into CD133+ and CD133- fractions. Total RNA was extracted from CD133+ cells and analyzed using the nCounter GX Cancer Reference kit, the Stem Cell panel and the custom made ITESM CodeSet from NanoString Technologies. This series contains data for the ITESM CodeSet.
2016-02-06 | E-GEOD-77614 | biostudies-arrayexpress
Project description:We investigated the role of breast cancer stem-like cells (CSCs-like), isolated from primary tumor, in promoting bone metastases in a human-in-mice model. Luciferase-transduced CD44+CD24- breast CSCs-like were injected through subcutaneous (SC) and intracardiac (IC) route in nonobese/severe combined immunodeficient (NOD/SCID) mice carrying subcutaneous human bone implants. The implanted bone was viable, active and human neo-vascularization was present. By in vivo luciferase imaging, we monitored tumor growth and detected bone-localized breast CSCs-like, both after SC and IC injection. Bone metastatic lesions were histologically evident, and tumor cells expressed epithelial markers and vimentin. Bone metastatic cells isolated from bone implants showed a CD44-CD24+ phenotype and re-created tumors and bone metastases after injection in secondary mice. A “bone tropism” expression signature was found to distinguish bone-colonizing cells from parental CSCs-like and to persist at subsequent passages also in the absence of surrounding bone tissue. The bone tropism signature displayed significant enrichment in genes discriminating bone metastases of breast cancer from metastases at other organs. Our results demonstrate the ability of breast CSCs-like to promote bone metastasis and provide a CSCs-like bone tropism signature, with potential prognostic value. C10 breast cancer stem-like cells (CSCs-like) were derived as mammospheres from a lobular-infiltrating breast carcinoma (ER+, HER2-). Samples are organized in the following groups: (i) Breast CSCs-like (C10, duplicate); (ii) Luciferase-transduced CSCs-like (C10L, simplicate); (iii) Bone-isolated C10L metastatic cells (C10-bone, duplicate) and subsequently (iv) grown in vitro as spheroids (C10-CSC, simplicate) or (v) re-grown in subcutaneous implants (C10-SC, duplicate).
2013-11-30 | E-GEOD-36102 | biostudies-arrayexpress
Project description:Cancer stem cells (CSCs) drive prostate cancer (PCa) progression and metastasis. These cells exhibit remarkable self-renewal, chemoresistant and invasive potentials, and are thought to participate in the changes in cellular architecture that lead to epithelial-to-mesenchymal transition (EMT). Conventional therapies fail to eliminate CSCs, which results in tumor recurrence and progression to castration resistant PCa (CRPC). Recent evidence suggests that castration itself can induce EMT, which could potentiate the “stemness” and number of CSCs within the tumor. Hence, there is an urgent need for EMT- and CSC-targeted therapies that could prevent progression to CRPC. 22Rv1, DU145, LNCaP, and PC3 cells were grown under sphere-forming conditions standardized in our lab. We have previously demonstrated that these enriched PCa cell lines exhibit phenotypic characteristics associated with CSCs in vivo. Over-expression of the stem-associated CD133 biomarker was determined via flow cytometric analysis. Total RNA was isolated from CD133+ prostasphere-derived cells. Gene expression profiling was carried out using the nCounter NanoString system and three different CodeSets associated with cancer or stem cells. Functional annotation was performed using the over-representation analysis tool from ConsensusPathDB. Functional annotation analysis of upregulated transcripts suggests that prostasphere-derived cells undergo a transcriptional reprogramming that triggers a major phenotypic shift. These changes are similar to the mesenchymal shift associated with EMT that drives PCa progression to CRPC. Each cell line exhibited distinct expression profiles that are presented and analyzed individually. Furthermore, our analysis revealed over-represented pathways that were common to all cell lines, which are related to the MAPK/ERK, PI3K/AKT, Notch, and Wnt stem cell fate signaling networks. Transcriptional analysis of induced CSCs not only offers insight into their underlying pathophysiology, but can also be used as a platform for the discovery of therapeutic targets for CSC-specific intervention. In this contribution, we present a flexible in vitro platform for the identification of functionally relevant therapeutic targets, using cell samples with low numbers of malignant stem/progenitors that were enriched in vitro. This approach represents a novel and effective strategy that can be used in the development of therapeutic strategies, which could ultimately be tailored to the biology of individual patients.
2016-02-06 | GSE77614 | GEO
Project description:Cancer stem cells (CSCs) drive prostate cancer (PCa) progression and metastasis. These cells exhibit remarkable self-renewal, chemoresistant and invasive potentials, and are thought to participate in the changes in cellular architecture that lead to epithelial-to-mesenchymal transition (EMT). Conventional therapies fail to eliminate CSCs, which results in tumor recurrence and progression to castration resistant PCa (CRPC). Recent evidence suggests that castration itself can induce EMT, which could potentiate the “stemness” and number of CSCs within the tumor. Hence, there is an urgent need for EMT- and CSC-targeted therapies that could prevent progression to CRPC. 22Rv1, DU145, LNCaP, and PC3 cells were grown under sphere-forming conditions standardized in our lab. We have previously demonstrated that these enriched PCa cell lines exhibit phenotypic characteristics associated with CSCs in vivo. Over-expression of the stem-associated CD133 biomarker was determined via flow cytometric analysis. Total RNA was isolated from CD133+ prostasphere-derived cells. Gene expression profiling was carried out using the nCounter NanoString system and three different CodeSets associated with cancer or stem cells. Functional annotation was performed using the over-representation analysis tool from ConsensusPathDB. Functional annotation analysis of upregulated transcripts suggests that prostasphere-derived cells undergo a transcriptional reprogramming that triggers a major phenotypic shift. These changes are similar to the mesenchymal shift associated with EMT that drives PCa progression to CRPC. Each cell line exhibited distinct expression profiles that are presented and analyzed individually. Furthermore, our analysis revealed over-represented pathways that were common to all cell lines, which are related to the MAPK/ERK, PI3K/AKT, Notch, and Wnt stem cell fate signaling networks. Transcriptional analysis of induced CSCs not only offers insight into their underlying pathophysiology, but can also be used as a platform for the discovery of therapeutic targets for CSC-specific intervention. In this contribution, we present a flexible in vitro platform for the identification of functionally relevant therapeutic targets, using cell samples with low numbers of malignant stem/progenitors that were enriched in vitro. This approach represents a novel and effective strategy that can be used in the development of therapeutic strategies, which could ultimately be tailored to the biology of individual patients.
2016-02-06 | GSE77612 | GEO