Gene expression profiling of murine renal adenocarcinoma cells during recursive implantations
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE142109 | GEO | 2021/10/27
REPOSITORIES: GEO
Similar Datasets
Project description:The mouse renal cancer cell line RENCA was serially passaged in vivo using multiple implantation strategies (called Kidney, Tail and Lung) designed to replicate different aspects of primary tumour growth and metastasis. We have acquired methylomic data.
2021-10-27 | GSE139338 | GEO
Project description:Tumors can occur in many sites in the body, but how tissues at different anatomical sites affect tumor microenvironments and their subsequent response to therapy is not known. Here we show that different tissues can cause the same tumor to develop fundamentally different microenvironments resulting in dramatic changes in responses to immunotherapy. Whereas established subcutaneous tumors could be eradicated in the majority of mice using a combination of three agonist antibodies, tumors in visceral organs responded much less. Orthotopic kidney tumors had a microenvironment with a higher frequency of alternatively-activated macrophages and their associated molecules. Neutralizing the CCL2 chemokine or IL-13 cytokine, important in macrophage biology led to a greatly improved therapeutic effect. Importantly, a significantly reduced therapeutic response of subcutaneous tumors was observed when visceral tumors were simultaneously present in the same mice. In this study we sought to compare gene expression of mouse renal cell carcinoma cells growing in the kidney to cells growing subcutaneously. Renca is a renal cell carcinoma cell line (Murphy and Hrushesky, 1973). To produce subcutaneous tumors, mice received 2 x 10^5 Renca. Orthotopic tumors were established by first surgically isolating the organ and then injecting 2 x 10^5 Renca cells intrakidney (IK) into the outer cortex of the kidney in 20 ul of PBS. Tumors were removed from mice 12 days after implantation, when approximately 20-30 mm2. Tumors were snap frozen on liquid nitrogen prior to processing for total RNA followed by analysis on Mouse Gene 1.0 chips. Kidney Renca tumors were excised from 3 BALB/c mice and subcutaneous Renca tumors were excised from another 3 BALB/c mice. cDNA was prepared and hybridized to Mouse Gene 1.0 ST chips.
2012-09-08 | E-GEOD-40679 | biostudies-arrayexpress
Project description:The origin and the contribution of breast tumor heterogeneity to its progression are not clear. We investigated the effect of a growing orthotopic tumor formed by an aggressive estrogen receptor (ER)-negative breast cancer cell line on the metastatic potential of a less aggressive ER-positive breast cancer cell line for the elucidation of how the presence of heterogeneous cancer cells might affect each other’s metastatic behavior. ER positive ZR-75-1/GFP/puro cells, resistant to puromycin and non-tumorigenic/non-metastatic without exogenous estrogen supplementation, were injected intracardiacally into mice bearing growing orthotopic tumors, formed by ER negative MDA-MB-231/GFP/Neo cells resistant to G418. A variant cell line B6, containing both estrogen-dependent and -independent cells, were isolated from GFP expressing cells in the bone marrow and re-inoculated in nude mice to generate an estrogen-independent cell line B6TC.
2011-05-25 | E-GEOD-27515 | biostudies-arrayexpress
Project description:Tumors can occur in many sites in the body, but how tissues at different anatomical sites affect tumor microenvironments and their subsequent response to therapy is not known. Here we show that different tissues can cause the same tumor to develop fundamentally different microenvironments resulting in dramatic changes in responses to immunotherapy. Whereas established subcutaneous tumors could be eradicated in the majority of mice using a combination of three agonist antibodies, tumors in visceral organs responded much less. Orthotopic kidney tumors had a microenvironment with a higher frequency of alternatively-activated macrophages and their associated molecules. Neutralizing the CCL2 chemokine or IL-13 cytokine, important in macrophage biology led to a greatly improved therapeutic effect. Importantly, a significantly reduced therapeutic response of subcutaneous tumors was observed when visceral tumors were simultaneously present in the same mice. In this study we sought to compare gene expression of mouse renal cell carcinoma cells growing in the kidney to cells growing subcutaneously. Renca is a renal cell carcinoma cell line (Murphy and Hrushesky, 1973). To produce subcutaneous tumors, mice received 2 x 10^5 Renca. Orthotopic tumors were established by first surgically isolating the organ and then injecting 2 x 10^5 Renca cells intrakidney (IK) into the outer cortex of the kidney in 20 ul of PBS. Tumors were removed from mice 12 days after implantation, when approximately 20-30 mm2. Tumors were snap frozen on liquid nitrogen prior to processing for total RNA followed by analysis on Mouse Gene 1.0 chips.
2012-09-08 | GSE40679 | GEO
Project description:The aim of the present study was to investigate the potential role of HIF-2a in regulating RCC susceptibility to natural killer (NK) cell-mediated killing. We demonstrated that the RCC cell line 786-O with mutated VHL was resistant to NK-mediated lysis as compared to the VHL corrected cell line (WT7). This resistance was independent of immunological synapse formation and NK ligand expression but was found to be reliant on HIF-2a stabilization in 786-0 cells. In order to elucidate the molecular basis of HIF-2a-induced impairment of NK-mediated killing, we performed global gene analysis using DNA microarray. Three candidate genes (ANGPTL4, ADM and ITPR1) were selected on the basis of their fold change and their involvement in cell death and survival. SiRNA targeting of these genes revealed that only ITPR1 silencing resulted in a significant increase of 786-O susceptibility to NK-mediated lysis. Using gene silencing of HIF2-a and chromatin immunoprecipitation assay, we showed for the first time that ITPR1 was a direct novel target of HIF2-a. Notably, a strong and significant correlation was found between ITPR1and HIF2-a staining in RCC patients. Transcriptional profiling of ITPR1silenced RCC cells indicated that several important genes involved in cell survival and apoptosis were differentially regulated. Using ITPR1 silenced Renca cells, we further found that ITPR1 was involved in the control of tumor progression. Moreover ITPR1 targeting combined with NK depletion significantly enhanced tumor growth as compared to ITPR1 knocked down Renca xenografts. Our data provide insights into the link between HIF-2a, ITPR1-related pathway and natural immunity and suggest a role of the HIF2/ITPR1 axis in regulating RCC cell survival.
2014-01-11 | E-MTAB-1802 | biostudies-arrayexpress
Project description:We have developed a progression series of increasingly metastatic cell lines generated from the normal mammary epithelial cell line, NMuMG, to distinguish between early changes in cancer initiation and metastasis-promoting alterations.
2017-06-17 | GSE94637 | GEO
Project description:Owing to the risk of insertional mutagenesis, viral transduction has been increasingly replaced by nonviral methods to generate induced pluripotent stem (iPS) cells. We report the use of ‘minicircle’ DNA, a vector type that is free of bacterial DNA and capable of high expression in cells. Here we use a single minicircle vector to generate transgene-free iPSCs from adult human adipose stem cells. (Note: Our Nature Methods publication included analysis of array data from GSM374067 and GSM374068 in conjunction with this series).
2010-02-01 | GSE20014 | GEO
Project description:In this study, we aimed to evaluate the effect of M2-like macrophages in the injured kidney on kidney cancer progression. As an acute kidney injury to chronic kidney disease model, we used unilateral ischemia-reperfusion injury (uIRI). And we inoculated RenCa cells, which are murine kidney cancer cell line, into renal subcapsule 14 days after uIRI (uIRI-Can) and compared uIRI-Can to RenCa cells inoculated into sham-operated renal subcapsule (Sham-Can) 20 days after inoculation. To identify gene characteristics of M2-like macrophages that are commonly detected both in the uIRI kidney cortex and uIRI-Can, we sorted Ly6Clow macrophages from 4 groups, uIRI kidney cortex, sham kidney cortex, uIRI-Can, and Sham-Can, and conducted RNA-Seq. This study revealed the characteristic gene expression of M2-like macrophages which were commonly detected in the injured kidney cortex and kidney cancer progressed on the injured kidney. And this could be a future therapeutic target of macrophage-targeted therapy.
2022-12-06 | GSE197494 | GEO
Project description:Owing to the risk of insertional mutagenesis, viral transduction has been increasingly replaced by nonviral methods to generate induced pluripotent stem (iPS) cells. We report the use of ‘minicircle’ DNA, a vector type that is free of bacterial DNA and capable of high expression in cells. Here we use a single minicircle vector to generate transgene-free iPSCs from adult human adipose stem cells. (Note: Our Nature Methods publication included analysis of array data from GSM378832 (Foreskin), GSM378833-GSM378838 (JT-iPSC), and GSM378817-GSM378820 (H1, H7, H9, H13, H14) in conjunction with this series).
2010-02-01 | GSE20033 | GEO
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