Transcriptomic analyses of co-treatment of AFB1 and curcumin in chicken liver
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ABSTRACT:
PROVIDER: PRJNA622813 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11472191_1.fastq.gz | Fastqsanger.gz | |||
| SRR11472191_2.fastq.gz | Fastqsanger.gz | |||
| SRR11472192_1.fastq.gz | Fastqsanger.gz | |||
| SRR11472192_2.fastq.gz | Fastqsanger.gz | |||
| SRR11472193_1.fastq.gz | Fastqsanger.gz |
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Project description:Purpose:In order to assess the toxicity of AFB1 in chicken liver and the mechanism of curcumin alleviating AFB1-induced liver toxicity in chicken, we established a co-administered model to investigate LncRNA and mRNA profiles of chicken liver. Methods: RNA extracted by Total RNA Extractor (Trizol) was utilized to construct the final library. Libraries were pooled and sequenced on a 150-bp paired-end Illumina HiSeq™ 2000 run. The sequencing data obtained from Illumina Hiseq™ was filtered to get clean reads using Trimmomatic. The reads themselves and their matching reads which length was less than 35nt were removed. Clean reads were aligned to the reference sequence (Gallus_gallus-5.0, NCBI) using HISAT2. Results: Sampling directly from the liver yielded sufficient quantities of RNA to assess transcripts from each chicken and mapped to 24,883 Gallus gallus genes. Conclusions: We used the method of RNA-seq to find the target genes and related signaling pathways involved in the co-administered (AFB1 and curcumin) and their underlying mechanisms.
2022-04-02 | GSE148014 | GEO
Project description:Aflatoxin B1 (AFB1) is extremely carcinogenic and can cause liver cancer in humans and animals with continued ingestion. As a natural compound, curcumin (Cur) exhibits excellent anti-inflammatory, and anti-cancer properties with few side effects. In this study, a total of 60 male mice (6-week-olds, 15 per group). After one week of acclimatization feeding, the mice were divided into control group (Con), AFB1 group, curcumin group (Cur), and AF+Cur group. The mice were gavaged with curcumin (Cur, 100 mg/kg) and/or AFB1 (0.75 mg/kg). To identify a new therapeutic target for AFB1-induced pyroptosis, we performed proteomic profiling for curcumin alleviating liver injury caused by AFB1 to further validate the targets through volcano plot analysis, Venn analysis, heatmap analysis, correlation, cluster analysis, GO and KEGG enrichment. AFB1 exposure resulted in the loss of hepatocyte membrane, swelling of the endoplasmic reticulum, and a significant increase in transaminase (ALT and AST) contents, while curcumin greatly improved these changes. We found that differentially expressed proteins are enriched in the endoplasmic reticulum membrane and identified ITPR2 as a target of curcumin that alleviates AFB1-induced liver injury by proteomics. Furthermore, ITPR2 expression was detected by immunofluorescence, and qRT-PCR for mRNA expression of genes downstream of ITPR2 (calpain1, calpain2, caspase-12, caspase-3). ITPR2-activated endoplasmic reticulum stress-related proteins (calpain1, calpaini2, bcl-2, BAX, cl-caspase-12, cl-caspase-3), apoptosis (PARP) and pyroptosis (DFNA5) related proteins were examined by western blotting. The analysis showed that it effectively prevents AFB1-induced pyroptosis by lowering endoplasmic reticulum stress via interfering with ITPR2 and its downstream proteins (calpain1, calpain2, bcl-2, Bax) and inhibiting caspase-12/caspase-3 pathway. Conclusively, this study applied proteomic profiling to elucidate ITPR2 as a new target, which might give a new perspective on the mechanism of curcumin alleviating AFB1-induced pyroptosis.
2023-05-21 | PXD042376 | iProX
Project description:Purpose:In order to assess the respiratory toxicity of co-infection in chicken lung, we established a co-infection model to investigate transcriptome profiles of chicken lung. Methods: RNA extracted by Trizol reagent (Invitrogen) was utilized to construct the final library (BGISEQ-500 RNA-Seq Library) based on the manufacturer’s instructions. Library was validated on the Agilent Technologies 2100 bioanalyzer. The library was amplified with phi29 to make DNA nanoball (DNB) which had more than 300 copies of one molecule. The DNBs were load into the patterned nanoarray and single end 50 bases reads were generated in the way of sequenced by synthesis. Whole transcriptome sequencing data was filtered and mapped to Chicken genome (Gallus genome Version 5.0.1 NCBI). DEG-seq method was based on Poisson distribution (Fold Change > 2 and Adjusted P value < 0.001) Results: Sampling directly from the lung yielded sufficient quantities of RNA to assess transcripts from each chicken and mapped to 18,043 Gallus gallus genes. Conclusions: We used the method of RNA-seq to find the target genes and related signaling pathways involved in the co-infection (MG and E.coli) and their underlying mechanisms.
2019-04-19 | GSE130015 | GEO
Project description:Background Clinical practice demonstrates that anticancer drug effects may strongly vary between different patients. Individual responses to drug action are potentially responsible for adverse effects such as establishment of resistance. Consequently, the understanding of response mechanisms to drug actions is of great relevance. Proteome profiling is a powerful tool for the investigation of cellular responses to drugs. Methods Here, we have investigated the effects of curcumin, a natural remedy with known anti-cancer activities, on breast cancer cells MCF-7, ZR-75-1 and normal mammary fibroblasts as well as co-cultures thereof using proteome profiling. The mammary fibroblasts had been treated before with TGF-beta in order to induce a wound-healing signature known to be representative for the in vivo situation in breast tumors. Results While co-culture alone induced several proteins like ANXA1, S100A4 and SPARC similarly in both breast cancer cells, the majority of proteins regulated upon co-culture differed between MCF-7 and ZR-75-1. Curcumin significantly induced HMOX1 in all single cell models and co-cultures. However, otherwise the curcumin effects differed. In the MCF-7 co-culture, curcumin significantly downregulated RC3H1, a repressor of inflammatory signaling. In the ZR-75-1 co-culture, curcumin significantly downregulated PEG10, an anti-apoptotic protein, and induced RRAGA, a pro-apoptotic protein involved in TNF-alpha signaling. In this model, curcumin also induced AKR1C2, an important enzyme for progesterone metabolism. None of these specific curcumin effects were observed in single cell cultures. Conclusions The present data demonstrate that curcumin induces proteome alterations potentially accounting for its known antitumor effects in a strongly context-dependent fashion.
2018-06-04 | PXD008719 | Pride
Project description:Transcriptomic analyses of co-infection of Mycoplasma gallisepticum and Escherichia coli in chicken lungs
| PRJNA533596 | ENA
Project description:Curcumin metabolite by Human Liver Microsomes in vitro.
2019-03-19 | MSV000083596 | MassIVE
Project description:The cancer stem cells (CSCs) have important therapeutic implications for multi-resistant cancers including hepatocellular carcinoma (HCC). Among the key pathways frequently activated in liver CSCs is NF-kB signaling. Here we evaluated the CSCs-depleting potential of NF-kB inhibition in liver cancer achieved by IKK inhibitor curcumin and specific peptide SN50 . The effects on CSCs were assessed by analysis of Side Population (SP) and expression levels of CSC-related genes as determined by RT-qPCR, gene expression microarray, EMSA, and Western blotting. Curcumin caused anti-proliferative and pro-apoptotic responses directly related to the extent of NF-kB inhibition. In curcumin-sensitive tumor cells, the treatment led to a selective CSC depletion as evidenced by a reduced SP size, decreased sphere formation, down-regulation of CSC markers and suppressed tumorigenicity. Similarly, NF-kB inhibition by SN50 caused a general suppression of cell growth accompanied by a reduced SP fraction. In contrast, curcumin-resistant cells exhibited a paradoxical increase in proliferation and expression of CSC markers. Mechanistically, CSC-depleting activity of curcumin was exerted by the NF-kB-mediated HDAC inhibition causing down-regulation of c-MYC and other key oncogenic targets. Co-administration of the class I/II HDAC inhibitor trichostatine sensitized resistant cells to curcumin. Further, integration of a predictive signature of curcumin sensitity with our HCC database indicated that HCC patients with poor prognosis and progenitor features are most likely to benefit from NF-kB inhibition. These results demonstrate that NF-kB inhibition can specifically target CSC populations and suggest a potential for combined inhibition of NF-kB and HDAC signaling for treatment of liver cancer patients with poor prognosis. Five human hepatoma cell lines with and without curcumin
2015-12-31 | E-GEOD-59713 | biostudies-arrayexpress
Project description:This dataset has been generated to identify promoter regions in the chicken genome to distinguish active and inactive genes. We focussed our analyses on actively transcribed tRNA and mRNAs genes. Chicken liver was cross-linked to capture histone-DNA interactions. Sequencing libraries were prepared from H3K4me3-precipitated DNA and input control.
2021-02-04 | E-MTAB-8106 | biostudies-arrayexpress
Project description:Oxidative stress as a result of cigarette smoking is an important etiological factor in the pathogenesis of chronic obstructive pulmonary disease (COPD), a chronic steroid-insensitive inflammatory disease of the airways. The activity of the transcriptional co-repressor Histone deacetylase-2 (HDAC2) is dramatically reduced in COPD and cells exposed to oxidative stress or cigarette smoke. Moreover, curcumin (diferuloylmethane), a dietary polyphenol, at concentrations upto 1uM specifically restores cigarette smoke extract (CSE)- or oxidative stress- impaired HDAC2 activity. The aim of this study was to therefore identify any links through those gene sets that are affected by oxidative stress and subsequent treatment with curcumin in order to determine whether or not this could explain the impact of curcumin on restoration of oxidant impaired HDAC2 transcriptional co-repressor activity. Keywords: time course
2008-03-20 | GSE10896 | GEO
Project description:The cancer stem cells (CSCs) have important therapeutic implications for multi-resistant cancers including hepatocellular carcinoma (HCC). Among the key pathways frequently activated in liver CSCs is NF-kB signaling. Here we evaluated the CSCs-depleting potential of NF-kB inhibition in liver cancer achieved by IKK inhibitor curcumin and specific peptide SN50 . The effects on CSCs were assessed by analysis of Side Population (SP) and expression levels of CSC-related genes as determined by RT-qPCR, gene expression microarray, EMSA, and Western blotting. Curcumin caused anti-proliferative and pro-apoptotic responses directly related to the extent of NF-kB inhibition. In curcumin-sensitive tumor cells, the treatment led to a selective CSC depletion as evidenced by a reduced SP size, decreased sphere formation, down-regulation of CSC markers and suppressed tumorigenicity. Similarly, NF-kB inhibition by SN50 caused a general suppression of cell growth accompanied by a reduced SP fraction. In contrast, curcumin-resistant cells exhibited a paradoxical increase in proliferation and expression of CSC markers. Mechanistically, CSC-depleting activity of curcumin was exerted by the NF-kB-mediated HDAC inhibition causing down-regulation of c-MYC and other key oncogenic targets. Co-administration of the class I/II HDAC inhibitor trichostatine sensitized resistant cells to curcumin. Further, integration of a predictive signature of curcumin sensitity with our HCC database indicated that HCC patients with poor prognosis and progenitor features are most likely to benefit from NF-kB inhibition. These results demonstrate that NF-kB inhibition can specifically target CSC populations and suggest a potential for combined inhibition of NF-kB and HDAC signaling for treatment of liver cancer patients with poor prognosis.
2015-12-31 | GSE59713 | GEO