Effect of CXCR4 knockdown in CAFs on gene expression
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE101082 | GEO | 2019/04/03
REPOSITORIES: GEO
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Project description:Purpose: The goals of this study are to invsetigate the primary signaling pathway enriched in CAFs after stimulation of LUAD supernatants. Methods: Briefly, the supernatants (HNRNPK knockdown and control) of H1299 cells were incubated with CAFs for 24h. Then the CAFs were used to extract total RNAs for quality control and RNA-seq loading samples. RNA-seq was performed as DGE on an Illumia HiSeq platform and 50 bp paired-end reads were generated (BGI Co. Ltd.). Results: Gene Ontology (GO) analysis revealed that cell proliferation and migration were identified as the biological functions of HNRNPK Conclusions: In CAFs, we confirmed that the PI3K-AKT signaling pathway was significantly enriched after stimulation of H1299 supernatants.
2022-03-02 | GSE197540 | GEO
Project description:RNA-seq (CAFs stimulated with control or HNRNPK knockdown supernatants)
| PRJNA810860 | ENA
Project description:The pregnant decidua is infiltrated by many immune cells which are thought to originate in the bone marrow (BM) promoting pregnancy. CXCR4 is a key regulator of the development of NK cells and dendritic cells, both of which play an important role in early placental development and immune tolerance at the maternal-fetal interface. However, the role of CXCR4 in pregnancy is not well understood. To generate tamoxifen-inducible CXCR4 knockout mice, we used the Cre/LoxP tamoxifen-inducible system. For animal experiments, Cre+/CXCR4fl/fl mice and their Cre-/CXCR4fl/fl littermates were used. After tamoxifen treatment, we refer to Cre-/CXCR4fl/wt mice as WT (wild type), and Cre+/CXCR4fl/null mice as CXCR4 KO (knockout). For adoptive bone marrow transplant (BMT) experiments, BMT was performed from either WT GFP transgenic male donor mice into WT or CXCR4 KO females, or from CXCR4 KO male donors into CXCR4 KO females as negative control. Collectively, our study found an important role for maternal CXCR4 expression in immune cell function, placental development and pregnancy maintenance.
2023-12-20 | GSE241958 | 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. 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:Effect of CXCR4 knockdown in CAFs on gene expression
| PRJNA393687 | ENA
Project description:CXCR4 cDNA transcripts were subcloned into plenti-IRES-GFP vectors, and stably transduced using a lentiviral system In addition to wild-type CXCR4, vectors with the mutations c.1013C>G (p.Ser338*), c.932_933insT (p.Thr311fs), and c.1030_1041delinsGT (p.Ser344fs) were generated. Cell lines were stimulated with 50nM of the CXCR4 ligand CXCL12 (SDF1A) (R&D Systems, Minneapolis MN) for two hours. RNA from each sample was extracted at baseline and at 2 hours.
2016-06-10 | GSE83150 | 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:The goal of this study was to identify signalling molecules downstream of CXCR4 in breast cancer cells. For this purpose, we sorted CXCR4-positive and CXCR4-negative cells from MDA-MB-231 breast cancer cell line by flow cytometry and performed microarrays analysis. Three sets of samples, each in quadruplicate, were analyzed. These include CXCR4-positive subpopulation, CXCR4-positive subpopulation treated with SDF-1 (ligand for CXCR4, also called CXCL12) for one hour and CXCR4-negative subpopulation.
2010-04-28 | E-GEOD-15893 | biostudies-arrayexpress
Project description:Ovarian cancer (OC) remains the leading cause of death in patients with gynecological malignancy. An improved understanding of the genomics has led to the separation of OC into histologically and molecularly defined subgroups. Based on molecular profiling in OC patients, subtype with a reactivated tumor stroma presented the worst prognosis, emphasizing the importance of tumor microenvironment especially stromal fibroblasts in fueling OC progression. Dicer1 is well recognized as the microRNA (miR) synthesis machinery, playing a crucial role in cellular maturation and development, and was generally considered to be a tumor suppressor gene that inhibited tumor initiation and metastasis. Dicer1 expression pattern and exact biological function was seldom studied in the stromal compartment. There was a recent study demonstrating that Dicer1 was involved in mouse embryonic fibroblast (MEF) development and maturation. Therefore, we are inspired to explore the expression and function of Dicer1 in stromal fibroblasts of OC patients. In this study, mRNA and microRNA gene expression profiling were conducted for MRC5-CAFs after silencing of Dicer1. By comparing the expression data of MRC5-CAFs transfected with control siRNA (si-Ctrl) or with Dicer1 specific siRNA (si-Dicer1) for 72 hr, we identified a set of differential expressed mRNA and microRNA in MRC5-CAFs after Dicer1 knockdown. This study was the first to investigate Dicer1 influence of stromal fibroblast gene expression and the underlying regulation mechanism, which held great importance in complementing our understanding of Dicer1 in OC initiation and development, and raises potent therapeutical targets in controlling OC metastasis We used microarrays to profile the mRNA expression of MRC5-CAFs before and after Dicer1 knockdown, in order to identify molecular alteration exerted by Dicer1 in the context of stromal fibroblasts.
2018-04-10 | GSE97936 | GEO