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Unknown,Transcriptomics,Genomics,Proteomics

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Regulation of gene expression by GLIPR1 in prostate cancer cells

ABSTRACT: Human glioma pathogenesis-related protein 1 (GLIPR1) and its mouse counterpart, Glipr1 are downregulated in prostate cancer (PCa) and other malignant cell lines, owing partly to methylation in the gene’s regulatory region. Loss of Glipr1 function predisposed mice to tumorigenesis. Restoration of GLIPR1 expression in prostate cancer cells and other malignant cells led to growth suppression and/or apoptosis. Here we show that restoring GLIPR1 expression in PCa cells leads to downregulated c-myc and cell cycle-related c-myc target genes, leading to the inhibition of cell cycle progression. DNA microarray (Illumina HumanHT-12) Prostate cancer cells were transduced with adenovirus-mediated GLIPR1 or control lacZ, grown in complete medium for 24 hours, synchronized by serum starvation for 24 hours, followed by serum restimulation for 30 min. RNA was prepared and subjected to DNA microarray analysis.

ORGANISM(S): Homo sapiens

SUBMITTER: Timothy Thompson

PROVIDER: E-GEOD-32367 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Regulation of gene expression by GLIPR1 in prostate cancer cells

Project description:Human glioma pathogenesis-related protein 1 (GLIPR1) and its mouse counterpart, Glipr1 are downregulated in prostate cancer (PCa) and other malignant cell lines, owing partly to methylation in the gene’s regulatory region. Loss of Glipr1 function predisposed mice to tumorigenesis. Restoration of GLIPR1 expression in prostate cancer cells and other malignant cells led to growth suppression and/or apoptosis. Here we show that restoring GLIPR1 expression in PCa cells leads to downregulated c-myc and cell cycle-related c-myc target genes, leading to the inhibition of cell cycle progression.

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Peripheral blood proteomic signature of newly diagnosed prostate cancer

Project description:Prostate cancer (PCa) is the most common malignant tumour, with high incidence rates and heterogeneity in men around the world. It is becoming an increasing burden on the health care system due to lack of tests for precise detection of disease, risk assessment and response to treatments. We used SWATH-MS as a discovery proteomics tool to identify markers in the serum of newly diagnosed PCa patients and healthy controls to facilitate the improved diagnosis. Furthermore, identification and expression of proteins was also determined in patients undergone radiotherapy and prostatectomy for monitoring of the clinical response to respective treatment options. Thus, this study provides the basis for a proteomic signature to improve diagnostics of patients with localised prostate cancer.

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Urinary endogenous peptides as biomarkers for prostate cancer

Project description:Prostate cancer (PCa) is one of the most prevalent cancer types in men worldwide. However, the main diagnostic tests available for PCa have limitations and need biopsy for histopathological confirmation of the disease. The prostate-specific antigen (PSA) is the main biomarker used for PCa early detection, but an elevated serum concentration is not cancer-specific. Therefore, there is a need for discovery of new non-invasive biomarkers that can accurately diagnose PCa. Here, we used trichloroacetic acid-induced protein precipitation and liquid chromatography-mass spectrometry to profile endogenous peptides in urine samples from patients with PCa (n = 33), benign prostatic hyperplasia (n = 25), and healthy individuals (n = 28). Receiver operating characteristic (ROC) curves were performed to evaluate the diagnostic performance of urinary peptides. In addition, proteasix tool was used for in silico prediction of protease cleavage sites. We found five urinary peptides derived from uromodulin significantly altered between the study groups, all of which were less abundant in the PCa group. In addition, urinary peptides outperformed PSA in discriminating between malignant and benign prostate conditions (AUC = 0.847), showing high sensitivity (81.82%) and specificity (88%). Overall, our study allowed the identification of urinary peptides with potential for use as non-invasive biomarkers in PCa diagnosis.

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Expression profiling of prostate cell lines by miRNA array

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Project description:Despite the clinical benefit of androgen-deprivation therapy (ADT), the majority of patients with advanced prostate cancer (PCa) ultimately develop lethal castration-resistant prostate cancer (CRPC). In this study, we identified thioesterase superfamily member 6 (THEM6) as a marker of ADT resistance in PCa. In patients, THEM6 expression correlates with progressive disease and is associated with poor survival. THEM6 deletion reduces in vivo tumour growth and restores castration sensitivity in orthograft models of CRPC. Mechanistically, THEM6 is located at the endoplasmic reticulum (ER) membrane and controls lipid homeostasis by regulating intracellular levels of ether lipids. As a consequence, THEM6 loss in CRPC cells significantly alters ER function, preventing lipid-mediated induction of ATF4 and reducing de novo sterol biosynthesis. Finally, we show that THEM6 is required for the establishment of the MYC-induced stress response. Thus, similar to PCa, THEM6 loss significantly impairs tumorigenesis in the MYC-dependent subtype of triple negative breast cancer. Altogether our results highlight THEM6 as a novel component of the treatment-induced stress response and a promising target for the treatment of CRPC and MYC-driven cancer.

2021-12-11 | PXD024407 | Pride

THEM6-mediated lipid remodelling sustains stress resistance in cancer (Part3 : THEM6 KO in LNCaP AI)

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THEM6-mediated lipid remodelling sustains stress resistance in cancer (Part2 : THEM6 KO in 22rv1)

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Expression data of LNCaP and MDA PCa 2b cells in absence or presence of IL6

Project description:Prostate cancer (PCa) development and progression are associated with chronic inflammation. The cytokine interleukin (IL)-6 can influence progression, differentiation, survival, and angiogenesis of PCa. To identify novel pathways that are triggered by IL-6, we performed a gene expression profiling of two PCa cell lines, LNCaP and MDA PCa 2b, under treatment with 5 ng/ml IL-6. Interferon regulatory factor (IRF)9 was identified as one of the most prevalent IL-6 regulated genes in both cell lines. IRF9 is a mediator of type I interferon signaling and acts together with signal transduction and activator of transcription (STAT)1 and 2 to activate transcription of interferon responsive genes. The IL-6 regulation of IRF9 was confirmed at mRNA and protein levels by quantitative real-time PCR and Western blot, respectively, in both cell lines and could be blocked by the anti-IL-6 antibody Siltuximab. Three PCa cell lines with an autocrine IL-6 loop, PC3, DU145, and LNCaP-IL-6+, showed a high expression of IRF9. A tissue microarray with 36 malignant and adjacent 36 benign areas from prostate cancer specimens showed that IRF9 protein expression is moderately elevated in malignant areas and positively correlates with the tissue expression of IL-6. Downregulation and overexpression of IRF9 provided evidence for an interferon-independent role of IRF9 on cellular proliferation of different PCa cell lines. Furthermore, expression of IRF9 was essential to mediate the antiproliferative effects of IFN-M-NM-12. We concluded that IL-6 is an inducer of IRF9 expression in prostate cancer and a sensitizer for the antiproliferative effects of IFNM-NM-12. LNCaP and MDA PCa 2b cells were seeded in 12 wells each. The cells were starved for 24 h and half were treated with 5 ng/ml IL-6 for 18 h. Two biological replicates were performed, each in three replicates, resulting in 12 samples per cell line.

2013-08-02 | E-GEOD-47973 | biostudies-arrayexpress

Expresssion data from primary mouse prostate tumor cells (primary prostate tumor cells; PPC, shrunken prostate tumor cells; S-PC, castration-resistant prostate tumor cells; CRPC)

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