RNA sequence analysis to compare mouse breast CAFs with and without targeted radiation at 6 day
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE172399 | GEO | 2022/04/20
REPOSITORIES: GEO
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Project description:RNA sequence analysis to compare mouse breast CAFs with and without targeted radiation at 6 day
| PRJNA723222 | ENA
Project description:Pancreatic ductal adenocarcinoma (PDAC) has a characteristically dense stroma comprised predominantly of cancer associated fibroblasts (CAFs). CAFs promote tumor growth, metastasis and treatment resistance. We aimed to investigate the molecular changes and functional consequences associated with chemotherapy treatment of PDAC CAFs. Chemoresistant immortalized CAFs (R-CAFs) were generated by continuous incubation in 100nM gemcitabine. Gene expression differences between treatment naïve CAFs (N-CAFs) and R-CAFs were compared by array analysis. Immortalized human pancreatic CAFs were grown for 30 days in either control media or media containing 100nM gemcitabine. RNA was then isolated and hybidized on U133 Plus 2.0 Affymetrix arrays.
2016-03-09 | E-GEOD-78982 | biostudies-arrayexpress
Project description:Data generrated shows that Dll1 has several genes upregulated after targeted radiation at day 30 inlcuding EMT, ROS etc
2022-04-20 | GSE172398 | GEO
Project description:Purpose: Tumor radioresistance can be driven by ERK phosphorylation and its downstream targets. In this context, melanomas harboring constitutive MAPK/ERK activation have been considered for targeted radionuclide therapy (TRT) with a radiolabeled melanin tracer ([131I]ICF01012), alone or in combination with MEK inhibitors (MEKi). Experimental design: We used three dimensional (3D) melanoma spheroid models to evaluate the effects of TRT in combination with MEKi, in human BRAFV600E SK-MEL-3, NRASQ61K 1007 and WT B16F10 murine melanomas. TRT was assessed in vivo using the syngeneic model C57Bl5/NRAS 1007 for biodistribution, dosimetry, efficiency and molecular mechanisms. Results: In spheroids, TRT cooperated with MEKi to increase apoptosis in both BRAF- and NRAS-mutant models that were resistant to TRT-induced apoptosis. However NRASQ61K spheroids were highly radiosensitive towards [131I]ICF01012-TRT. Actually, mice bearing NRAS1007 melanoma and receiving 18.5MBq of [131I]ICF01012 had a significant extended survival (median: 92 vs 44 days, p < 0.0001), associated with a 93 Gy tumor deposit, leading to a dramatic decrease of tumor growth. Furthermore, the number of lymph node metastases was reduced in mice receiving [131I]ICF01012. Comparative transcriptomic analyses confirm a decrease of mitosis, proliferation and metastasis signature in TRT-treated tumors vs control tumors. These analyses also suggest that in this NRAS-melanoma, TRT acts through an increase of oxidation and inflammation as well as P53 activation. Conclusions: Our data support the view that combining [131I]ICF01012-TRT with MEKi can be of benefit for the treatment of advanced pigmented BRAF-mutant melanoma. Likewise, [131I]ICF01012 alone can be considered as a new potential NRAS-mutant melanoma treatment.
2021-03-31 | GSE162536 | GEO
Project description:Pancreatic ductal adenocarcinoma (PDAC) has a characteristically dense stroma comprised predominantly of cancer associated fibroblasts (CAFs). CAFs promote tumor growth, metastasis and treatment resistance. We aimed to investigate the molecular changes and functional consequences associated with chemotherapy treatment of PDAC CAFs. Chemoresistant immortalized CAFs (R-CAFs) were generated by continuous incubation in 100nM gemcitabine. Gene expression differences between treatment naïve CAFs (N-CAFs) and R-CAFs were compared by array analysis.
2016-03-09 | GSE78982 | GEO
Project description:Hepatocellular carcinoma (HCC) is a malignancy that is challenging to treat. Cancer-associated fibroblasts (CAFs) are reported to promote the malignant behavior of HCC cells via cytokines. Conophylline (CnP) has been reported to suppress activated hepatic stellate cells in liver fibrosis. We aimed to determine whether CnP is useful in suppressing tumor growth in HCC. We investigated whether CnP could suppress the HCC-promoting effect of CAFs derived from HCC tissues in vitro and in vivo. CAFs promoted the proliferation and invasion of HCC cells. CnP suppressed activated CAFs expressing α-smooth muscle actin (αSMA) and inhibited the HCC-promoting effects of CAFs. CnP significantly reduced the levels of cancer-promoting cytokines such as interleukin (IL)-6 (IL-6), IL-8, C-C Motif Chemokine Ligand 2 (CCL2), angiogenin, and osteopontin, which are secreted by CAFs. An in vivo study demonstrated that combined therapy with CnP and sorafenib against CAFs and HCC cells showed the strongest inhibition of tumor growth compared with the control and single treatment groups. Transcriptome analysis revealed that GPR68 in CAFs was strongly suppressed by CnP. The cancer-promoting effects of cytokines were eliminated by knockdown of GPR68 in CAFs. CnP inhibited the HCC-promoting effect of CAFs by suppression a number of HCC-promoting cytokines, which are secreted from CAFs expressing GPR68. Combination therapy with CnP and existing anti-cancer agents may be a promising therapeutic strategy in overcoming refractory HCC with activated CAFs.
2022-01-01 | GSE140530 | GEO
Project description:To understand the molecular mechanisms that underpin pro-tumourigenic functions of cancer-associated fibroblasts (CAFs) we compared the proteome, acetylome, phosphoproteome of human immortalised breast cancer CAFs with those of the normal mammary fibroblasts that they were generated from. Based on the results obtained, we have also analysed proteome changes when CAFs were treated with the P300/CBP inhibitor c646.
2022-04-10 | PXD018343 | Pride
Project description:To identify miRNA differentially expressed in CAFs vs matched NFs and analyze the heterogeneity of miRNA expression profiles in the two kinds of cells, we established primary cultures of CAFs and paired NFs from six resected breast tumor tissue without any radiotherapy and chemotherapy treatment. Paired CAFs and NFs from six primary human breast carcinoma specimens were cultured,the third passage of primary cells was used in the experiments.
2012-09-28 | E-GEOD-37527 | biostudies-arrayexpress
Project description:Background: Androgen deprivation therapy (ADT) is the backbone of therapy for advanced prostate cancer (PCa). Despite the good initial response, castration resistance and metastatic progression will inevitably occur. Cancer-associated fibroblasts (CAFs) may be implicated in promoting metastasis of PCa after ADT. Our aim is to investigate the role and mechanism of CAF-derived exosomes involving in metastasis of PCa after ADT. Methods: PCa cells were co-cultured with exosomes derived from DHT-treated or ETOH-treated CAFs, and their migration and invasion differences under castration condition were examined both in vitro and in vivo. The miRNA profiles of exosomes derived from DHT-treated CAFs and matched ETOH-treated CAFs were analysed via next generation sequencing. The transfer of exosomal miR-146a-5p from CAFs to PCa cells was identified by fluorescent microscopy. The function and direct target gene of exosomal miR-146a-5p in PCa cells were confirmed through Transwell assays, luciferase reporter, and western blot. Findings: Compared with DHT-treated CAFs, exosomes derived from ETOH-treated CAFs dramatically increase migration and invasion of PCa cells under castration condition. MiR-146a-5p level in exosomes from ETOH-treated CAFs was significantly reduced. The loss of miR-146a-5p may strengthen the epithelial-mesenchymal transition (EMT) to accelerate cancer cells metastasis by modulating epidermal growth factor receptor (EGFR)/ERK pathway. Interpretation: CAFs-derived exosomal miR-146a-5p confers metastasis in PCa cells under ADT through the EGFR/ERK pathway and it may present a new treatment for PCa.
2022-08-02 | GSE154215 | GEO
Project description:This study aims to identify genes differentially expressed in oral CAFs with respect to their normal counterparts, i.e. oral NFs. We collected oral normal mucosal tissues and oral squamous cell carcinoma (OSCC) tissues from 12 healthy people and 12 OSCC patients, respectively, at West China Hospital of Stomatology, Sichuang University, P. R. China. The tissues were isolated, cultured and purified using standard protocols to obtain oral NFs and CAFs. Agilent 4×44K Whole Genome Oligo Microarrays were used to measure the gene expression profiles of the samples. Sample preparation and hybrid reactions were performed according to the manufacture’s instructions. RNA samples from NFs and CAFs were pooled respectively before hybridization. The chips were scanned and visualized using the Agilent DNA microarray scanner. Probe set intensities were measured using Agilent Feature Extraction software (version 10.5.1.1). Raw data were normalized in the Agilent GeneSpring GX software (version 11.0) using the Agilent FE one-color scenario (mainly median normalization). Oral NFs and CAFs were obtained from tissues derived from 12 healthy people undergoing plastic surgery and 12 OSCC patiens undergoing surgical resection. RNA samples from NFs and CAFs were pooled respectively before hybridization.
2012-01-26 | E-GEOD-35356 | biostudies-arrayexpress