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Diffusible factors released from human prostate carcinoma cells restrained cancer stem cells from contributing to tumor progression

ABSTRACT: The growth and progression of many cancers is thought to be driven by small subpopulations of cancer stem cells (CSC). Long-term cultures of CSC have been established to develop therapeutic strategies aimed at eradicating these tumorigenic cells. To evaluate the contribution of CSC to the progression of prostate cancer we isolated a CD44+CD24- tumor cell population from the DU145 cell line, derived from a brain metastasis of human prostate carcinoma, and established their CSC properties. The behaviour of selected CSC was then investigated with respect to the bulk DU145 cells. Interestingly, CSC were able to generate very aggressive tumors in immunodeficient mice, but this capacity was interfered by the presence of differentiated DU145 cells, resulting in the growth of scarcely aggressive tumors. To understand the influence of DU145 cells on CSC we performed co-culture experiments, demonstrating that signals released from differentiated tumor cells interfered with CSC acquisition of an aggressive phenotype. Our findings highlight that the fate of prostate CSC can be controlled by microenvironmental signals that restrain CSC from contributing to prostate cancer progression. Finally, we identified several molecules possibly involved in this cell-to-cell signaling, hypothesizing their potential value as novel prognostic markers or therapeutic targets.

ORGANISM(S): Homo sapiens

PROVIDER: GSE28313 | GEO | 2013/03/01

SECONDARY ACCESSION(S): PRJNA139327

REPOSITORIES: GEO

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Diffusible factors released from human prostate carcinoma cells restrained cancer stem cells from contributing to tumor progression

Project description:The growth and progression of many cancers is thought to be driven by small subpopulations of cancer stem cells (CSC). Long-term cultures of CSC have been established to develop therapeutic strategies aimed at eradicating these tumorigenic cells. To evaluate the contribution of CSC to the progression of prostate cancer we isolated a CD44+CD24- tumor cell population from the DU145 cell line, derived from a brain metastasis of human prostate carcinoma, and established their CSC properties. The behaviour of selected CSC was then investigated with respect to the bulk DU145 cells. Interestingly, CSC were able to generate very aggressive tumors in immunodeficient mice, but this capacity was interfered by the presence of differentiated DU145 cells, resulting in the growth of scarcely aggressive tumors. To understand the influence of DU145 cells on CSC we performed co-culture experiments, demonstrating that signals released from differentiated tumor cells interfered with CSC acquisition of an aggressive phenotype. Our findings highlight that the fate of prostate CSC can be controlled by microenvironmental signals that restrain CSC from contributing to prostate cancer progression. Finally, we identified several molecules possibly involved in this cell-to-cell signaling, hypothesizing their potential value as novel prognostic markers or therapeutic targets. To investigate the cellular response involved in tumorigenesis both at the level of gene expression and at the pre-mRNA splicing level we performed a whole genome microarray analysis of two paradigmatic experimental conditions, DU145 cells and their selected CSC.

2013-03-01 | E-GEOD-28313 | biostudies-arrayexpress

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Glucose Metabolic Remodeling through Phosphoenolpyruvate Carboxykinase Isoform 2 Regulates Prostate Cancer Cell Tumorigenicity

Project description:Patients with aggressive prostate cancer generally present with poor outcomes. Identifying the factors regulating prostate cancer aggressiveness may open new avenues in therapy. Specifically, information from prostate cancer patient databases revealed that higher phosphoenolpyruvate carboxykinase isoform 2 (PCK2) levels correlate with more aggressive tumors and lower survival rates. Herein, we show that high tumorigenic prostate cancer cell clones express high levels of PCK2. We found that elevated levels of PCK2 are critical for the glucose metabolic remodeling and the maintenance of tumor-initiating cells (TICs) in aggressive prostate cancer. Our data suggest that PCK2 promotes tumorigenicity by lowering acetyl-CoA levels through reducing the mitochondrial tricarboxylic acid (TCA) cycle. Thus, PCK2 is a potential therapeutic target for aggressive prostate cancer. 2 subclones have been isolated from DU145 cells. The epithelial like (EL) clone has a high tumorigenicity ability and enriched tumor initiating cells than mesenchymal like (ML) clone. Genes with differential expression pattern between these two clones were detected by gene micorarray.

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Genome wide analysis of important transcription factors and histone modifications for prostate cancer progression

Project description:Prostate cancer is the most common cancer in men and androgen receptor (AR) downstream signalings promote prostate cancer progression. Although androgen deprivation therapy is effective for treating prostate cancer, most tumors relapsed as castration-resistant prostate cancer (CRPC). We performed ChIP-seq analysis to investigate the role of important transcription factors and histone modifications using AR positive prostate cancer cells, LNCaP, CRPC model cells, 22Rv1 and DU145 cells.

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SWATH proteomic profiling of prostate cancer cells identifies NUSAP1 as a biomarker of response to Galiellalactone

Project description:Galiellalactone (GL) is a fungal metabolite that presents antitumor and anti-inflammatory activities in vitro and in vivo. Previous studies have shown that GL targets NF-KB and STAT3 pathways and induces G2/M cell cycle arrest in androgen-insensitive prostate cancer cells. In this study, we show that GL-induced cell cycle arrest is independent of the NF-KB and STAT3 pathways in DU145 and PC-3 cells, and also that GL did not affect cell cycling in androgen-sensitive prostate cancer cell such as LNCaP and 22Rv1 cells. In addition, we showed confluence resistance to GL in DU145 cells. Using a SWATH proteomic approach we identified the down-regulation of Nucleolar and spindle associated protein 1 (NUSAP1) under DU145 confluence and in LNCaP cells. Also, the inhibition of NUSAP1 by siRNAs induced resistance to GL in DU145 cells, suggesting that NUSAP1 may be a target for GL and could be useful as biomarker for responsiveness of the antitumor activity of GL.

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Project description:Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. Although initially hormone-deprovation therapy is effective to inhibit cancer progression, most of cancers relapse as castration-resistant prostate cancer (CRPC). In this study, we examined the effect of OCT4 or NRF1 knockdown in CRPC cells. In order to investigate the OCT4 and NRF1 function in CRPC cells, we performed gene expression in AR-positive CRPC cell line, 22Rv1, AR-negative CRPC cell lines, PC3-CR (Cabazitaxel resistant), DU145, and DU145-CR, after siOCT4 (10 nM) or siNRF1 (10 nM) treatment. We also treated cells with vehicle, ribavirin (riba), or dihydrotestosterone (DHT) to analyzed the effects of thiese drug treatments.

2021-05-01 | GSE146656 | GEO

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Project description:DU145 human prostate cancer cells were injected into the prostate of nude mice and cells metastasizing to lymph node (LN1) grown and experiment repeated to make LN2-4. DU145 human prostate cancer cells were injected into the tail vein of nude mice and cells metastasizing to lung (ivLU1) grown and experiment repeated to make ivLU2-4.

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Monitoring In Vitro Response of Selenium-Treated Prostate Cells by 1H NMR Spectroscopy

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