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Berberine mitigates 5-fluorouracil-induced intestinal mucosal damage without impairing anti-tumor effect of 5-Fu by regulating the intestinal flora

ABSTRACT: Berberine mitigates 5-fluorouracil-induced intestinal mucosal damage without impairing anti-tumor effect of 5-Fu by regulating the intestinal flora

PROVIDER: PRJNA889331 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21857743_1.fastq.gz	Fastqsanger.gz
	SRR21857743_2.fastq.gz	Fastqsanger.gz
	SRR21857744_1.fastq.gz	Fastqsanger.gz
	SRR21857744_2.fastq.gz	Fastqsanger.gz
	SRR21857745_1.fastq.gz	Fastqsanger.gz

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Berberine mitigates 5-fluorouracil-induced intestinal mucosal damage without impairing anti-tumor effect of 5-Fu by regulating the intestinal flora

Project description:To investigate the mechanism of BBR improved intestinal mucosa induced by 5-fluorouracil-induced in mice

2024-08-15 | GSE215201 | GEO

5-Fluorouracil-induced intestinal mucositis via nuclear factor-κB activation

Project description:5-Fluorouracil (5-FU) is a commonly used drug for the treatment of malignant cancers. However, approximately 80% of patients undergoing 5-FU treatment suffer from gastrointestinal mucositis. The aim of this report was to identify the critical molecule involved in 5-FU-induced intestinal mucositis. Our data showed that 5-FU induced inflammation in the small intestine, characterized by the increased intestinal wall thickness and crypt length and the decreased villus height. Network analysis of 5-FU-affected genes by transcriptomic tool showed that the expression of genes was regulated by nuclear factor-κB (NF-κB), and NF-κB was the central molecule in the 5-FU-regulated biological network. NF-κB activity was activated by 5-FU in the intestine, which was judged by bioluminescence imaging and immunohistochemical staining. However, 5-aminosalicylic acid (5-ASA) inhibited 5-FU-induced NF-κB activation and proinflammatory cytokine production. Moreover, 5-FU-induced histological changes were improved by 5-ASA. In conclusion, our findings suggested that NF-κB was the critical molecule associated with the pathogenesis of 5-FU-induced mucositis, and inhibition of NF-κB activity ameliorated the mucosal damage caused by 5-FU.

2017-02-09 | GSE28873 | GEO

Analysis of gene expression profile in 5-fluorouracil (5-FU)-resistant human colon cancer cells

Project description:We analyzed the differentially regulated genes in 5-fluorouracil-resnstant human colon cancer cells to discover novel biomarkers involved in 5-FU resistance in colorectal cancer.

2017-03-27 | GSE56322 | GEO

Impact of 5-FU on the proteome of HEK293T cells

Project description:In this study, we wanted to examine the effects of 5-fluorouracil, a drug used in anticancer treatment, on the proteome of HEK293T cells (human cell culture). HEK293T cells were exposed to 5-fluorouracil (5-FU) using two different incubation strategies. In the first experiment, cells were incubated in 5-FU supplied medium and harvested after 24h acute exposure. The second experiment included a 24h exposure to 5-FU, followed by a recovery phase, were cells were incubated for another 6h in fresh medium without 5-FU. We performed shotgun proteomics of the respective tryptic digest of both experiments and compared the proteome of treated and untreated cells, respectively.

2025-03-18 | PXD051672 | Pride

5- FU treated organoids

Project description:5-Fluorouracil (5-FU) is a chemotherapeutic drug component that is commonly used for the treatment of solid cancers. The anticancer properties of 5-FU have been attributed to interference with nucleotide synthesis and through direct incorporation into the DNA as being a pyrimidine analog. As both mechanisms of action may have a mutational impact on surviving tumor cells, we performed three independent analyses to characterize the genomic consequences of 5-FU treatment: i) in vitro treatment of intestinal organoids with 5-FU followed by whole genome sequencing, ii) genome-wide mutation analyses in tumor samples from 5-FU treated patients with breast or colorectal cancer, and iii) analysis of paired biopsies from patients treated with 5-FU between biopsies. Our results demonstrate that both in vitro and in vivo 5-FU causes a mutational pattern that is dominated by T>G substitutions in a CTT context and with strong resemblance to COSMIC signature 17. Interestingly, this signature is also found in non 5-FU treated patients, most prominently in esophageal tumors, indicating that distinct endogenous and exogenous triggers can converge into highly similar mutational signatures. Furthermore, our results suggest that 5-FU may have adverse mutagenic effects on healthy cells and contributes to genetic variability in surviving cancer cells thereby contributing to tumor evolution.

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Gene expression of HCT116 colorectal cancer cells after treament with Thymoquinone (TQ), 5-Fluorouracil (5-FU), Combination of the individual compounds (Combi) and the Hybrid compound (SARB).

Project description:Cancer stem cells (CSCs) residing in colorectal cancer tissues have tumorigenic capacity and contribute to chemotherapeutic resistance and disease relapse. It is well known that the survival of colorectal CSCs after 5-Fluorouracil (5-FU)-based therapy leads to cancer recurrence. Thus CSCs represent a promising drug target. Here, we designed and synthesized novel hybrid molecules linking 5-FU with the plant-derived compound thymoquinone (TQ) and tested the potential of individual compounds and their combination to eliminate colorectal CSCs. SARB hybrid showed augmented cytotoxicity against colorectal cancer cells. Data obtained via Nanostring nCounter Gene Expression Assay (Pan Cancer Pathway Panel). Nanostring analysis revealed a unique signature of dysregulated gene expression in response to the combination of TQ and 5-FU (Combi) and SARB treatment. Importantly, two principle stem cell regulatory pathways WNT/ß-Catenin and PI3K/AKT were found to be downregulated after hybrid treatment.

2018-11-24 | GSE122860 | GEO

Role of miR-19b and its target mRNAs on 5-fluorouracil resistance in colon cancer cells

Project description:Despite the efforts in defining the molecular mechanisms for the drug resistance in colorectal cancers, little is known about the roles of microRNAs. With microarray containing 723 microRNAs, we examined effect of 5-fluorouracil (5-FU) on the microRNA expression. Respond to 5-FU, we identify two microRNAs, miR-19b and miR-21, that were differentially expressed in 5-FU resistant colon cancer cells derived from KM12C and DLD-1.

2011-07-27 | GSE30894 | GEO

HSC 5-FU time course

Project description:HSC (Sca+ SP) were isolated from 8-12 week C57B6 mice at various time points after treatment with 5-Fluorouracil. RNA was isolated from 50,000-100,000 FACS sorted cells and subjected to two rounds of T7 based linear amplification using Ambion's Message Amp kit. Two replicates from each time point were analyzed. http://www.plosbiology.org/plosonline/?request=get-document&doi=10.1371%2Fjournal.pbio.0020301 Keywords = HSC Keywords = proliferation Keywords = quiescence Keywords = 5-FU Keywords: time-course

2004-09-28 | GSE1559 | GEO

Novel mechanisms of 5-Fluorouracil Resistance in Colorectal Cancer: A Proteomic Investigation

Project description:One of the main obstacles to therapeutic success in colorectal cancer (CRC) is the development of acquired resistance to treatment with drugs such as 5-fluorouracil (5-FU), the most commonly used drug in CRC patients. Whilst some mechanisms of resistance are well-known, it is clear from the stasis in therapy success rate, that much is still unknown. Here a proteomics approach is taken towards identification using 5-FU resistant sublines of human CRC cell lines generated in-house. Using a multiplexed stable isotope labelling with amino acids in cell culture (SILAC) proteomics strategy, the resistant cell lines, and equivalently passaged 5-FU-sensitive cell lines were compared to parent cell lines grown in Heavy medium using 2D liquid chromatography and Orbitrap Fusion™ Tribrid™ Mass Spectrometry analysis.

2024-06-16 | PXD047672 | Pride

Downregulation of KRAB zinc finger proteins in 5-fluorouracil resistant colorectal cancer cells

Project description:The radio-chemotherapy with 5-fluorouracil (5-FU) is the standard of care treatment for patients with locally advanced rectal cancer (LARC) but it is only effective for a third of them. The proteomic and transcriptomic response of three colorectal cancer (CRC) cell lines to 5-FU and radiation was assessed and correlated with their genetic background. The induction of a 5-FU-resistance in those cell lines negatively affects the levels of transcripts corresponding to Krüppel-associated box (KRAB)-containing zinc finger proteins (ZFPs), the largest family of transcriptional repressors. Among nearly 350 KRAB-ZFPs, almost a quarter are down-regulated after the induction of a 5-FU-resistance including a common one between the three CRC cell lines, ZNF649, whose role is still unknown. This proteomic, transcriptomic and genomic analysis of intrinsic and acquired resistance highlights possible new mechanisms involved in resistance to treatment and therefore potential new therapeutic targets to overcome this resistance.

2022-05-19 | PXD020000 | Pride

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