Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1012356 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25890128_1.fastq.gz | Fastqsanger.gz | |||
| SRR25890128_2.fastq.gz | Fastqsanger.gz | |||
| SRR25890129_1.fastq.gz | Fastqsanger.gz | |||
| SRR25890129_2.fastq.gz | Fastqsanger.gz | |||
| SRR25890130_1.fastq.gz | Fastqsanger.gz |
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Project description:Ginkgo biloba leaf extract (GBE) is used in traditional Chinese medicine as an herbal supplement for improving memory. Exposure of B6C3F1/N mice to GBE in a 2-year National Toxicology Program (NTP) bioassay resulted in a dose-dependent increase in hepatocellular carcinomas (HCC). To identify key microRNAs that modulate GBE-induced hepatocarcinogenesis, we compared the global miRNA expression profiles in GBE-exposed HCC (GBE-HCC) and spontaneous HCC (SPNT-HCC) with age-matched vehicle control normal livers (CNTL) from B6C3F1/N mice. The number of differentially altered miRNAs in GBE-HCC and SPNT-HCC were 74 (52 up and 22 down) and 33 (15 up and 18 down), respectively. Among the uniquely differentially altered miRNAs in GBE-HCC,, miR-31 was selected for functional validation. A potential miRNA response element (MRE) in the 3’-untranslated regions (3’-UTR) of Cdk1 mRNA was revealed by in silico analysis and confirmed by luciferase assays. In mouse hepatoma cell line HEPA-1 cells, we demonstrated an inverse correlation between miR-31 and CDK1 protein levels, but no change in Cdk1 mRNA levels, suggesting a post-transcriptional effect. Additionally, miRNA expression analysis in non-tumor liver samples from the 90-day GBE mouse study demonstrated an upregulation of miRs-411, 300, 127, 134, 409-3p, and 433-3p in GBE-exposed group compared to vehicle control group, indicating that some of these miRNAs could serve as potential biomarkers for GBE exposure or hepatocellular carcinogenesis. These data increase our understanding of miRNA-mediated epigenetic regulation of GBE-mediated hepatocellular carcinogenesis in B6C3F1/N mice.
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Project description:To get deeper insights into the GSH-triggered systemic defense signaling events in plants, we performed transcriptome profiling on leaf 6 collected after one hour application of GSH to leaf 1 of WT plants. To further investigate the relations between GSH and Glu in plant wound response, we generated transcriptome data sets from leaf 6 one hour after wounding leaf 1 or application of Glu to leaf 1 of WT plants.
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Project description:Purpose: To gain molecular insights of HBV integration that may contribute to HCC tumorigenesis, we performed whole transcriptome sequencing and whole genome copy number profiling of hepatocellular carcinoma (HCC) samples from 50 Chinese patients. Conclusions: This is the first report on the molecular basis of the MLL4 integration driving MLL4 over-expression. HBV-MLL4 integration occurred frequently in Chinese HCC patients, representing a unique molecular segment for HCC with HBV infection.
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Project description:<p>The ncRNA transcriptome of human hepatocellular carcinoma (HCC) is largely unexplored. We used CAGE to characterize transcription start sites across different etiologies of human HCCs with emphasis on ncRNAs. Here we report that retroviral LTR promoters, expressed in healthy tissues such as testis and placenta but not liver, are widely activated in HCC. Despite HCC heterogeneity, a subset of LTR-derived ncRNAs were more than 10-fold up-regulated in the vast majority of samples. HCCs with a high LTR activity mostly had a viral etiology, were less differentiated and showed higher risk of recurrence. CAGE enabled us to build a promoter map for HCC, which uncovers a new layer of complexity in HCC genomics.</p>
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Project description:We report the transcriptome difference between glandular cells of type VI trichome and leaf cells of trichome shaved leaf.
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Project description:A genome-wide integrated methylome and transcriptome analysis of the early stage of hepatocellular carcinoma development that induced by HBx. The HBV x (HBx) protein, which plays a critical role in the development of HCC, was shown to interact with several epigenetic factors, such as DNMT3A and HDAC1. Most HBx transgenic (TG) mice spontaneously develop HCC at about 1 year of age, providing genetic validation of the oncogenic potential of HBx even in the absence of viral integration and chronic inflammation. Therefore, it would be intriguing to study the regulatory role of HBx in the epigenome and its impact on HCC development. We performed a genome-wide analysis to examine the differences in DNA methylation patterns and RNA transcriptions between cancer and normal liver cells. High-throughput sequencing analysis of MIRA (methylated CpG island recovery assay) and mRNA at 3 mouth old age mouse liver
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Project description:transcriptome changes in pea leaves with sulfur deficency/sufficiency during reproductive phase.-Characterization of transcriptome changes in leaves of wild-type and PsSultr4 mutant lines (for a sulfur transporter) subjected or not to sulfur deficiency during the reproductive phase 4plex_pea_2014_01 - transcriptome changes in pea leaves with sulfur deficency/sufficiency during reproductive phase. - Role of sulfur and of the sulfate store in leaf metabolism. - Comparison of: 1- The leaf transcriptome of pea subjected or not to sulfur deficiency during the reproductive phase (S+ versus S –) 2- The leaf transcriptome of wild-type and mutant lines for a sulfur transporter (two TILLING alleles) grown under sulfur sufficient conditions : WT1/Mut1 S+ et WT2/Mut2 S+ 3- The leaf transcriptome of wild-type and mutant lines for a sulfur transporter (two TILLING alleles) grown under sulfur deficient conditions : WT1/Mut1 S+ et WT2/Mut2 S+
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Project description:An increasing number of non-coding RNAs (ncRNAs) are implicated in various human diseases including cancer; however ncRNA transcriptome of hepatocellular carcinoma (HCC) remains largely unexplored. We use CAGE (Cap Analysis of Gene Expression) to comprehensively map transcription start sites (TSSs) across different etiologies of human HCC as well as mouse HCC, with particular emphasis on ncRNAs distant from protein-coding genes. We find thousands of significantly up-regulated distal ncRNAs in HCC tumors compared to their matched non-tumors, which are as many as protein-coding genes. Moreover, we identify many LTR retroviral promoters activated in HCC tissues and expressed in a subfamily-specific manner, which account for approximately 20% of the up-regulated distal ncRNAs. The transcripts derived from LTRs, determined by 3' RACE, are multi-exon nuclear ncRNAs typically 0.5-2kb in length. This study sheds light on ncRNA transcriptome of human and mouse HCC. Expression profiles using CAGE for 37 mouse HCC. The human data are archived at dbGaP (phs000885.v1.p1). An umbrella BioProject has been created to associate the GEO and dbGaP BioProjects: PRJNA278792
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Project description:Plant productivity is adversely affected by exposure to abiotic stresses including salinity. Leaf tissue undergoes accelerated senescence with exposure to salt stress conditions, culminating in lowered efficiency of photosynthetic machinery. The N6-adenine derivative phytohormone Cytokinin (CK) is well known to delay natural leaf senescence by maintaining functioning photosynthesis processes. How various forms of CK function to control this activity and alter physiological and molecular responses under salt-induced leaf senescence is still not known. Here the CKs, trans-Zeatin (tZ) and its N-glucosylated (tZNGs) forms; tZ7G and tZ9G, were tested for their ability to delay leaf senescence in Arabidopsis thaliana. A modified dark-induced leaf senescence CK bioassay was used to study the physiology of photosynthesis performance as well as transcriptome and proteome level changes in detached leaves, across different phases of salt-induced leaf senescence from 2h-72h. Treatments with different CK forms (tZ, tZ7G, and tZ9G) showed that tZNGs can improve PSII efficiency (Fv/Fm) and increase chlorophyll levels compared to salt only treatments, indicating that these CK forms function as active CK forms in delaying senescence. At the transcript level, tZ, tZ7G, and tZ9G revealed differentially expressed genes (DEGs) across both developmental and salt-treated senescence, with tZNGs predominantly altering DEG in the terminal timepoint of salt-treated leaf senescence. Additionally, we found that tZNGs uniquely regulate crucial biological processes (BPs) including CK signaling compared to tZ. Proteome analysis showed that tZNGs and tZ showed similarities in number of differentially abundant proteins (DAPs) trends across senescence timepoints although each of the three forms showing uniquely abundant proteins. GO term analysis for tZNG regulated genes and proteins revel the enrichment of senescence- and chloroplast-related BPs. This study highlights the role of tZNGs as active cytokinin forms towards delaying salt-treated leaf senescence in Arabidopsis at the physiology, transcriptome, and proteome level.
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Project description:The identification of predictive markers to determine the premetastatic phase before metastasis is critical for developing effective strategies for early detection and prevention. By applying the dynamic network biomarker (DNB) approach to analyze time-series transcriptomic data from a pulmonary metastasis HCC mouse model, we revealed that the premetastatic phase occurred during the fourth week after implantation. A total of 142 DNB genes were identified as functionally important biomarkers of this critical phase, among which 60S ribosomal protein L6 (RPL6) was a core DNB member. RPL6 was significantly upregulated in HCC tissues with extrahepatic metastasis and was strongly correlated with poor prognosis in HCC patients. RPL6 promoted the invasion and metastasis of HCC cells, both in vitro and in vivo. Mechanistically, RPL6 directly bound to the HMGCS1 mRNA 3’UTR, a rate-limiting enzyme in cholesterol biosynthesis, thus increasing HMGCS1 mRNA stability and protein expression and subsequently elevating intracellular cholesterol level. Elevated cholesterol inhibited of the ubiquitin-dependent degradation of HIF-1α by binding to PHD2 and reducing PHD2-mediated hydroxylation of HIF-1α, which further resulted in HIF-1α signaling pathway activation. Moreover, RPL6, HMGCS1 and HIF-1α were coexpressed in HCC tissues with extrahepatic metastasis. Taken together, this study provides new insights into the dynamic transcriptome profiles of HCC pulmonary metastasis and establishes an important role for the RPL6-HMGCS1-HIF-1α axis in HCC metastasis, suggesting potential prognostic biomarkers and therapeutic targets in HCC.
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