MiRNA expression in the exosomes from oxaliplatin treated or not sw480 cells
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PROVIDER: PRJNA420932 | ENA |
REPOSITORIES: ENA
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Project description:detect miRNA expression in the exosomes isolating from the cell culture of sw480 cells treated by oxaliplatin or not
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2014-07-03 | E-GEOD-58027 | biostudies-arrayexpress
Project description:Drug resistance and distant metastases are leading causes of mortality in colorectal cancer (CRC), yet the molecular mechanisms linking these processes remain elusive. In this study, we demonstrate that acquired resistance to oxaliplatin, a first-line chemotherapeutic in CRC, enhances metastatic potential through transcriptional reprogramming. Using a clinically relevant dosing regimen, we generated oxaliplatin-resistant CRC cells that displayed increased metastatic potential. Integrated transcriptomic and phenotypic analyses revealed that dysregulated cholesterol biogenesis amplifies TGF-b signaling, which in turn drives expression of SERPINE1, that serves as a key effector of both oxaliplatin resistance and metastasis. Furthermore, we uncovered a SERPINE1-associated nine-gene expression signature, RESIST-M, that robustly predicts overall and relapse-free survival across distinct patient cohorts. Notably, RESIST-M stratifies a high-risk subtype of CMS4/iCMS3-fibrotic patients that display the poorest prognosis, underscoring its clinical relevance. Targeting of SERPINE1 or cholesterol biosynthesis re-sensitized resistant, pro-metastatic cells to oxaliplatin in mouse xenograft models. Altogether, this study uncovers a mechanistic link between metabolic rewiring and transcriptional plasticity underlying therapy-induced metastasis in primary CRC. Additionally, it also reveals actionable vulnerabilities that offer both prognostic value and therapeutic potential.
2025-07-23 | GSE299428 | GEO
Project description:Oxaliplatin-induced neuropathic pain is a common dose-limiting side effect of cancer treatment but the underlying mechanisms are largely unknown. The neuropathic pain model was established by oxaliplatin intraperitoneal administration for five consecutive days. In the present study, we performed whole genome expression microarray analysis by using spinal dorsal horn from oxaliplatin-treated and vehicle-treated rats on day 10.
2020-03-11 | GSE146739 | GEO
Project description:Introduction Chemotherapy, particularly with oxaliplatin, is a key treatment for advanced gastric cancer (GC), and exosomes derived from human bone marrow mesenchymal stem cells (hBM-MSCs) play a vital role in the tumor microenvironment. Objectives The study aims to elucidate the previously unexplored role of exosomes derived from hBM-MSCs in GC tumorigenesis, especially under the influence of chemotherapy. Methods We conducted an integrated study, utilizing miRNA sequencing and biological experiments, to analyze the tumorigenicity of exosomal miR-424-3p secreted by hBM-MSCs and its target gene RHOXF2 in GC cell lines. The results were confirmed through experimentation using a xenograft mouse model. Results This study demonstrated the role of hBM-MSCs in the GC microenvironment, focusing on their Epithelial-Mesenchymal Transition (EMT) facilitation through exosomes, which led to enhanced tumorigenicity of in GC cells. Intriguingly, this pro-tumor effect was abrogated when hBM-MSCs were treated with oxaliplatin. Exosomal miRNA sequencing revealed that oxaliplatin can upregulate the levels of miR-424-3p in exosomes secreted by hBM-MSCs, thereby inhibiting the EMT process in GC cells. Furthermore, miR-424-3p was identified to target and downregulate RHOXF2 expression, impeding the malignant behavior of GC cells both in vitro and in the mouse model. Conclusions These findings uncover a potential hidden mechanism of oxaliplatin's anti-tumor action and propose the delivery of miR-424-3p via exosomes as a promising avenue for anti-tumor therapy.
2023-11-30 | GSE248357 | GEO
Project description:ChIP-on-chip tilling array comparing untreated human SW480 cells vs SW480 cells treated with 2mM H2O2 for 30min. Exposing cells to the reactive oxygen species, hydrogen peroxide, recruits DNA methyltransferase 1 (DNMT1) to damaged chromatin. DNMT1 becomes part of a complex(es) containing DNMT3B and members of Polycomb Repressive Complex 4. The goal was to determine the effect of hydrogen peroxide treatment on chromatin, including changes in histone modifications and binding patterns of chromatin-associated proteins. [Agilent-014706]: Two-condition: untreated SW480 cells (U) vs H2O2 treated SW480 cells (T). Five-mark: SIRT1, gamma-HA2X, DNMT1, DNMT3B, and EZH2. [Agilent-014707]: Two-condition: untreated SW480 cells (U) vs H2O2 treated SW480 cells (T). Five-mark: SIRT1, gamma-HA2X, DNMT1, DNMT3B, and EZH2. [Agilent-026595]: Two-condition: untreated SW480 cells (U) vs H2O2 treated SW480 cells (T). Five-mark: SIRT1, gamma-HA2X, DNMT1, DNMT3B, and H3. [Agilent-027811]: Two-condition: untreated SW480 cells (U) vs H2O2 treated SW480 cells (T). Four-mark: H3, 3MeK4H3, AcK16H4, and 3MeK27H3.
2011-12-01 | E-GEOD-32382 | biostudies-arrayexpress
Project description:miRNA sequencing of NSC-released exosomes treated with metformin or not
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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