Ontology highlight
ABSTRACT:
PROVIDER: PRJNA703442 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13761457_1.fastq.gz | Fastqsanger.gz | |||
| SRR13761457_2.fastq.gz | Fastqsanger.gz | |||
| SRR13761458_1.fastq.gz | Fastqsanger.gz | |||
| SRR13761458_2.fastq.gz | Fastqsanger.gz | |||
| SRR13761459_1.fastq.gz | Fastqsanger.gz |
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Project description:Colorectal cancer (CRC) is closely related to gut dysbiosis. We investigated the effects of imbalanced gut microbiota on the progression of intestinal adenoma in Apcmin/+ mice model using fecal microbiota transplantation (FMT). Administration of feces from CRC patients increased tumor proliferation and decreased apoptosis in tumor cells. Abnormal expression of genes related to Wnt-protein binding and lipid metabolic process was observed.
2019-09-16 | GSE136682 | GEO
Project description:Several lines of evidence suggest that inflammation plays a pivotal role in the development and progression of CRC and can be unleashed by the loss of innate immunosurveillance. The complement system is a well characterized first line of defense against pathogens and a central component of the immune responses. As such, the complement system is an important determinant in the maintenance of intestinal homeostasis and emerging evidences suggest that complement dysregulation is involved in the development and progression of CRC. Here we show that in CRC patients CpG island methylation occurs in the gene encoding for the complement anaphylatoxin C3a receptor (c3aR) and strong C3aR down-regulation resulted in decreased overall survival and events-free survival in CRC patients. Ablation of c3ar in mouse models of CRC resulted in the establishment of a pro-inflammatory microbial flora, which fostered strong Th1/Th17 immune responses and a striking increase in tumor incidence and growth that were both dependent on the microbiota. Our findings highlight a previously unrecognized tumor oncosuppressive role for C3aR in CRC that could be exploited as a biomarker for more effective therapeutic intervention.
2020-02-01 | E-MTAB-8500 | biostudies-arrayexpress
Project description:The aim of this study was to test the hypothesis that replenishing the microbiota with a fecal microbiota transplant (FMT) can rescue a host from an advanced stage of sepsis. We developed a clinically-relevant mouse model of lethal polymicrobial gut-derived sepsis in mice using a 4-member pathogen community (Candida albicans, Klebsiella oxytoca, Serratia marcescens, Enterococcus faecalis) isolated from a critically ill patient. In order to mimic pre-operative surgical patient condition mice were exposed to food restriction and antibiotics. Approximately 18 hours prior to surgery food was removed from the cages and the mice were allowed only tap water. Each mouse received an intramuscular Cefoxitin injection 30 minutes prior to the incision at a concentration of 25 mg/kg into the left thigh. Mice were then subjected to a midline laparotomy, 30% hepatectomy of the left lateral lobe of the liver and a direct cecal inoculation of 200 µL of the four pathogen community. On postoperative day one, the mice were administered rectal enema. Mice were given either 1 ml of fecal microbiota transplant (FMT) or an autoclaved control (AC). This was again repeated on postoperative day two. Mice were then followed for mortality. Chow was restored to the cages on postoperative day two, approximately 45 hours after the operation. The injection of fecal microbiota transplant by enema significantly protected mice survival, reversed the composition of gut microflora and down-regulated the host inflammatory response. The cecum, left lobe of the liver, and spleen were isolated from mice for microarray processing with three or more replicates for six expermental conditions: non-treated control, SAHC POD1, SAHC.AC POD2, SAHC.FMT POD2, SAHC.AC POD7, SAHC.FMT POD7
2015-07-30 | E-GEOD-71530 | biostudies-arrayexpress
Project description:Group 3 innate lymphoid cells (ILC3s) are critical regulators of intestinal homeostasis, yet their role in cancer remains elusive. Here, we identify that the tumor microenvironment of humans and mice with colorectal cancer (CRC) contains altered ILC3 responses that resemble those found during intestinal inflammation and are characterized by reduced frequencies, altered subset distribution, and an imbalance with T cells. We evaluated the consequences of these changes in mice and determined that ILC3-specific major histocompatibility complex class II (MHCII) was required to limit the progression of CRC. Interestingly, ILC3-specific MHCII also prevented resistance to anti-PD-1 immunotherapy by regulating intestinal inflammation and microbiota composition. Finally, humans with intestinal inflammation and dysregulated ILC3s also harbor specific microbiota that are sufficient to promote immunotherapy resistance in mice. Collectively, these data define a protective role for antigen-presenting ILC3s in cancer, and indicate that inherent disruption of this pathway drives CRC progression and immunotherapy resistance.
2021-07-09 | GSE165814 | GEO
Project description:Colorectal Cancer (CRC) is one of most common cancers in the world and a main treatment in postoperative chemotherapy is oxaliplatin and fluorouracil (FOLFOX), But the effect is different among CRC patients. In this study, LC-MS/MS strategy was used to profile the plasma proteome in FOLFOX benefit and futile group. As a result, a panel of plasma proteins by machine learning from our data was verified for a possible prediction tool in postdiagnosis.
2024-05-21 | PXD044201 | Pride
Project description:Increasing importance in the onset and progression from colonic adenomatous polyps (AP) to colorectal cancer (CRC) has been attributed to the gut microbiota and the oncometabolites they may produce. To comprehensively study the microbial spatial variations and role of microbiota in CRC progression, multiple niches from the gastrointestinal system have to be investigated. We collected saliva, tissue and stool samples from 61 patients, including 46 CRC patients and 15 AP patients, well matched in age and sex, who were undergoing surgery in 2018 at the Careggi University Hospital (Florence, Italy). For all samples and locations we surveyed microbial composition through 16S ribosomal RNA and metabolites using NMR, and compared them across tissues and disease state, also considering CRC TNM staging. Our result suggest the importance of microbiota communities and derived oncometabolites in CRC development. Such association can be a forerunner for future studies on CRC/AP management.
2023-05-03 | GSE217490 | GEO
Project description:Purpose and Experimental Design: The purpose of this study is to find a methylation-related gene that could become a biomarker or therapeutic target in colorectal carcinoma (CRC). We screened candidate genes suspected to be silenced by DNA methylation using oligonucleotide microarray analysis. To investigate the clinical significance of one candidate gene (UNC5B), we analyzed the correlation between mRNA expression and clinicopathological features using clinical tissue samples. Finally, methylation specific PCR analysis was performed to reveal whether the promoter region was methylated in CRC cell lines. Results: We found 75 candidate genes that were potentially suppressed by DNA methylation in CRC. We focused on UNC5B, a possible tumor suppressor gene and regulator of apoptosis known to be inactivated in CRC. The mRNA expression analysis using tissue samples revealed that UNC5B mRNA was down-expressed in about 20% of CRC patients, and the patients with low-UNC5B-expression tumors showed a significantly higher recurrence rate after curative surgery. According to the univariate and multivariate analysis, low UNC5B expression was an independent risk factor for postoperative recurrence in stage I, II, and III CRC patients. Furthermore, patients with low expression of UNC5B in tumors had significantly poorer prognosis than those with high expression of UNC5B. Although UNC5B mRNA expression was restored by the demethylation treatment in CRC cell lines, the promoter region of UNC5B was not methylated. Conclusion: UNC5B is a potential biomarker for the selection of patients with high risk of postoperative recurrence and worse prognosis in CRC.
2011-12-04 | GSE22598 | GEO
Project description:At present, the mechanisms underlying the association between gut microbiota metabolites and immunotherapy in CRC remain unknown. Here, we conducted a multiomics analysis of a cohort of patients with mCRC and found that F.nucleatum was more abundant in patients who did not respond to immunotherapy. We also found that F. nucleatum diminished the sensitivity to anti-PD-1 mAb through its metabolite succinic acid. Accordingly, patients with lower serum succinic acid levels achieved a better response to immunotherapy. Mechanistically, F.nucleatum-derived succinic acid suppressed the cGAS-interferon-β pathway, consequently dampening the antitumor response by limiting CD8+ T-cell trafficking to the tumor microenvironment in vivo. Treatment with metronidazole reduced intestinal F.nucleatum abundance and thereby decreased serum succinic acid levels, thus resensitizing the tumors to immunotherapy in vivo. Collectively, our findings indicate that F. nucleatum and its metabolite succinic acid induce tumor resistance to immunotherapy and offer new insights into microbiota-metabolite-immune crosstalk in CRC.
2023-12-01 | GSE209864 | GEO
Project description:At present, the mechanisms underlying the association between gut microbiota metabolites and immunotherapy in CRC remain unknown. Here, we conducted a multiomics analysis of a cohort of patients with mCRC and found that F.nucleatum was more abundant in patients who did not respond to immunotherapy. We also found that F. nucleatum diminished the sensitivity to anti-PD-1 mAb through its metabolite succinic acid. Accordingly, patients with lower serum succinic acid levels achieved a better response to immunotherapy. Mechanistically, F.nucleatum-derived succinic acid suppressed the cGAS-interferon-β pathway, consequently dampening the antitumor response by limiting CD8+ T-cell trafficking to the tumor microenvironment in vivo. Treatment with metronidazole reduced intestinal F.nucleatum abundance and thereby decreased serum succinic acid levels, thus resensitizing the tumors to immunotherapy in vivo. Collectively, our findings indicate that F. nucleatum and its metabolite succinic acid induce tumor resistance to immunotherapy and offer new insights into microbiota-metabolite-immune crosstalk in CRC.
2023-10-01 | GSE181337 | GEO
Project description:Occurrence of Colorectal cancer（CRC）is relevant with gut microbiota. However, role of IRF3, a key signaling mediator in innate immune sensing, has been barely investigated in CRC. Here, we unexpectedly found that the IRF3 deficient mice are hyper-susceptible to the development of intestinal tumor in AOM/DSS and Apcmin/+ models. Genetic ablation of IRF3 profoundly promotes the proliferation of intestinal epithelial cells via aberrantly activating Wnt signaling. Mechanically, IRF3 in resting state robustly associates with the active β-catenin in the cytoplasm, thus preventing its nuclear translocation and cell proliferation, which can be relieved upon microbe-induced activation of IRF3. In accordance, the survival of CRC is clinically correlated with the expression level of IRF3. Therefore, our study identifies IRF3 as a negative regulator of the Wnt/β-catenin pathway and a potential prognosis marker for Wnt-related tumorigenesis, and describes an intriguing link between gut microbiota and CRC via the IRF3-β-catenin axis.
2020-09-16 | GSE155777 | GEO