Gene expression in PC3 cells(human prostate cancer cell line) upon HIC1 knockout
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ABSTRACT:
PROVIDER: PRJNA594285 | ENA |
REPOSITORIES: ENA
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Project description:To explore the role of HIC1 deletion in regulating prostate cancer(PCa) microenvironment development, Human Gene Expression Microarrays were searched for altered genes upon HIC1 knockout expression in PC3 cells. According to fold-change screening between HIC1-knockout and its respective control cells, both up-regulated and down-regulated genes were shown.
2019-12-10 | GSE141642 | GEO
Project description:This study aimed to further our understanding of the role that hypermethylatioted in cancer 1 (HIC1) plays in prostate cancer (PCa) development. Microarrays were searched for some genes that had correlated expression with HIC1 mRNA. Our data showed that HIC1 promoter hypermethylation was presented in cell lines, tissues and plasma of PCa patients. According to fold-change screening between restoring expression of HIC1 and its respective control cells, both up-regulated and down-regulated genes were commonly observed in PC3 and C4-2B cells. The restoring expression HIC1 in PCa lines were respectively noted as PC3-HIC1 and C4-2B-HIC1 cells, and the respective controls were noted as C4-2B-GFP and PC3-GFP cells.
2012-11-17 | E-GEOD-42336 | biostudies-arrayexpress
Project description:This study aimed to further our understanding of the role that hypermethylatioted in cancer 1 (HIC1) plays in prostate cancer (PCa) development. Microarrays were searched for some genes that had correlated expression with HIC1 mRNA. Our data showed that HIC1 promoter hypermethylation was presented in cell lines, tissues and plasma of PCa patients. According to fold-change screening between restoring expression of HIC1 and its respective control cells, both up-regulated and down-regulated genes were commonly observed in PC3 and C4-2B cells.
2012-11-17 | GSE42336 | GEO
Project description:To explore the role of HIC1 silencing in regulating PCa EMT development, Human Gene Expression Microarrays were searched for altered genes upon silencing HIC1 expression in C4-2B and DU145 cells. According to fold-change screening betweenHIC1-silenced and its respective control cells, both up-regulated and down-regulated genes were shown. Human PCa cell lines C4-2B and DU145 were transfected with lenti-virus (shRNA targeting HIC1 and respective control). HIC1-silenced cells were respectively noted as C4-2B-shHIC1 and DU145-shHIC1. Their respective control cells were respectively noted as C4-2B-shctrl and DU145-shctrl.
2016-03-03 | E-GEOD-78850 | biostudies-arrayexpress
Project description:In order to address the putative role of MELK and UBE2C in prostate cancer development and progression, we performed functional analysis upon siRNA-based knockdown, and searched for downstream genes and processes by microarray experiments. RNAi-based inhibition of MELK and UBE2C was efficient in PC3 prostate cancer cells and decreased transcriptional level down to about 30% remaining expression level. Illumina microarray experiments were done upon siRNA based knockdown 48h after transfection of PC3 cells in triplicates.
2012-10-19 | E-GEOD-32873 | biostudies-arrayexpress
Project description:To explore the role of HIC1 silencing in regulating PCa EMT development, Human Gene Expression Microarrays were searched for altered genes upon silencing HIC1 expression in C4-2B and DU145 cells. According to fold-change screening betweenHIC1-silenced and its respective control cells, both up-regulated and down-regulated genes were shown.
2016-03-03 | GSE78850 | GEO
Project description:In order to address the putative role of MELK and UBE2C in prostate cancer development and progression, we performed functional analysis upon siRNA-based knockdown, and searched for downstream genes and processes by microarray experiments. RNAi-based inhibition of MELK and UBE2C was efficient in PC3 prostate cancer cells and decreased transcriptional level down to about 30% remaining expression level.
2012-10-19 | GSE32873 | GEO
Project description:To study the effect of miR-130a in prostate cancer, PC3 cells overexpressing miR-130a were analyzed for global gene expression.
2017-03-10 | GSE80750 | GEO
Project description:BACKGROUND: Cancer stem-like cells are proposed to sustain solid tumors by virtue of their capacity for self-renewal and differentiation to cells that comprise the bulk of the tumor, and have been identified for a variety of cancers based on characteristic clonal morphologies and patterns of marker gene expression. METHODS: Single cell cloning and spheroid culture studies were used to identify a population of cancer stem-like cells in the androgen-independent human prostate cancer cell line PC3. RESULTS: We demonstrate that, under standard culture conditions, ~10% of PC3 cells form holoclones with cancer stem cell characteristics. These holoclones display high self-renewal capability in spheroid formation assays under low attachment and serum-free culture conditions, retain their holoclone morphology when passaged at high cell density, exhibit moderate drug resistance, and show high tumorigenicity in scid immunodeficient mice. PC3 holoclones readily form spheres, and PC3-derived spheres yield a high percentage of holoclones, further supporting their cancer stem cell-like nature. We identified one gene, FAM65B, whose expression is consistently up regulated in PC3 holoclones compared to paraclones, the major cell morphology in the parental PC3 cell population, and two genes, MFI2 and LEF1, that are consistently down regulated. This molecular profile, FAM65Bhigh/MFI2low/LEF1low, also characterizes spheres generated from parental PC3 cells. The PC3 holoclones did not show significant enriched expression of the putative prostate cancer stem cell markers CD44 and integrin α2β1. PC3 tumors seeded with holoclones showed dramatic down regulation of FAM65B and dramatic up regulation of MFI2 and LEF1, and unexpectedly, a marked increase in tumor vascularity compared to parental PC3 tumors, suggesting a role of cancer stem cells in tumor angiogenesis. CONCLUSIONS: These findings support the proposal that PC3 tumors are sustained by a small number of tumor-initiating cells with stem-like characteristics, including strong self-renewal and pro-angiogenic capability and marked by the expression pattern FAM65Bhigh/MFI2low/LEF1low. These markers may serve as targets for therapies designed to eliminate cancer stem cell populations associated with aggressive, androgen-independent prostate tumors such as PC3. (Mol Cancer. 2010 Dec 29;9:319. doi: 10.1186/1476-4598-9-319; PMID: 21190562; PMCID: PMC3024252).
2013-11-07 | GSE52161 | GEO
Project description:We found that PC3 cells secrete proteases that cleavae and activate PAR1 and PAR2. In order to understand gene regulation by this autocrine signaling loop, PAR1 and PAR2 knockout cell gene expression was compared to WT PC3 cell gene expression. Proteinase activated receptors (PARs) are G protein-coupled receptors (GPCRs) activated by limited N-terminal proteolysis. A variety of proteolytic enzymes derived from the coagulation cascade and inflammatory milieu activate PARs, however specific activators in different physiological and pathophysiological contexts remain poorly defined. PARs are highly expressed in many cancer cells and regulate various aspects of tumor growth and metastasis. Endogenous proteinases that regulate PARs in the setting of various tumors however remains unresolved. Prostate cancer (PCa) remains a major cause of mortality in men despite advances in early detection and clinical intervention. PAR expression has been reported in PCa, however, their role here remains poorly defined. In androgen independent PC3 cells, we find functional expression of PAR1 and PAR2 but not PAR4. Using genetically encoded PAR cleavage biosensors, we find that PCa cells secrete proteolytic enzymes that cleave PARs and trigger autocrine signaling. Deletion of PAR1 and PAR2 using CRISPR/Cas9 combined with microarray analysis revealed genes that are differentially regulated by this autocrine signalling mechanism. Interestingly, several genes that are known PCa prognostic factors or biomarker were differentially expressed in PAR1-KO and PAR2-KO PC3 cells. We also examined PAR1 and PAR2 regulation of PCa cell proliferation and migration using PAR1 and PAR2-KO PC3 cells, as well as PAR1 and PAR2 specific agonists and antagonists. We find that PAR1 and PAR2 have opposite effects on PC3 cell proliferation and migration. In summary, we have identified an autocrine signaling mechanism through PARs as a regulator of PCa cell function.
2022-08-24 | GSE211813 | GEO