Transcriptomic studies in NR4A1 overexpressing MIN6 cells and the effect of EGCG by RNA seq analysis
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ABSTRACT:
PROVIDER: PRJNA932737 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23372015_1.fastq.gz | Fastqsanger.gz | |||
| SRR23372015_2.fastq.gz | Fastqsanger.gz | |||
| SRR23372016_1.fastq.gz | Fastqsanger.gz | |||
| SRR23372016_2.fastq.gz | Fastqsanger.gz | |||
| SRR23372017_1.fastq.gz | Fastqsanger.gz |
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Project description:Overexpression of the epidermal growth factor receptor family member Her-2/neu in breast cancer leads to autophosphorylation of the receptor, and induction of multiple downstream signaling pathways including Akt kinase to NF-kappaB cascade that is associated with poor prognosis. Previously, we demonstrated green tea polyhenol epigallocatechin 3-gallate (EGCG) inhibits growth of NF639 Her-2/neu-driven breast cancer cells via reducing receptor autophosphorylation, and downstream Akt and NF-kappaB activities (Pianetti et al., 2002). Interestingly, we noted that upon prolonged culture in the presence of EGCG some cells developed resistance to the polyphenol. Here we report that resistant cells have lost tyrosine phosphorylation on the Her-2/neu receptor. Surprisingly, they displayed elevated NF-kappaB activity, and inhibition of this activity sensitized cells to EGCG. Data from microarray analysis of the original and resistant NF639 populations of cells were subjected to Gene Set Enrichment Analysis (GSEA) pathway analysis, which revealed that the mitogen activated protein kinase (MAPK) pathway was activated in the resistant cells. Treatment of the resistant cells with a combination of EGCG and the MAPK inhibitor U0216 dramatically reduced colony growth and mesenchymal phenotype. Thus, activation of the MAPK pathway mediates resistance to EGCG. Our studies suggest that gene expression profiling of drug resistant cells may provide a mechanism of determining effective systemic therapies for treatment of these advanced cancers. Keywords: Drug resistance
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Project description:To determine the impact of Hnf1a overexpression on gene expression in mouse beta cells, we performed RNA-seq experiments on MIN6 where Hnf1a was overexpressed using CRISPR activation (SAM system).
2022-05-01 | E-MTAB-11474 | biostudies-arrayexpress
Project description:Epigallocatechin gallate (EGCG), the major green tea polyphenol, has been a subject of global interest as a potential chemopreventive or chemotherapeutic supplement for breast cancer. While on one hand epidemiological studies suggest inverse correlation between green tea consumption and breast cancer risk, investigations using cell culture and animal models of breast carcinogenesis on the other hand have demonstrated antiproliferative, antitumor, anti-invasive and anti-metastatic properties of EGCG. Mechanism of how EGCG affects cell proliferation, apoptosis, migration and cell cycle by affecting the function of a wide range of molecular targets have also been studied. However, the question as to how EGCG impacts on estrogen responsive genes has not been addressed. This issue is of relevance to our notion of EGCG as a potential chemopreventive or chemotherapeutic agent against breast cancer, which is estrogen dependent in majority of the newly diagnosed cases. Here, using the estrogen receptor α (ERα) positive MCF-7 breast cancer cells as a model, we have examined the effect of EGCG on the estrogen regulated genes. MCF7 cells were treated with vehicle (Ethanol) or EGCG in the presence or absence of estrogen for 24hrs. Total RNA was extracted; Cy3 labeled cRNA was hybridized to Genotypic Technology designed Custom Human Whole Genome 8x60k Microarray (Agilent-027114). Median signal intensities were used for the analysis. After background subtraction (normexp) and normalization (quantile) differentially expressed genes were identified using linear models.
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Project description:To further explore the underlying molecular mechanism of GR’s effects, we transfected the Min6 cell with the GR cDNA expression vector or control vector, and then extracted RNA of Min6 cells. M6A antibody was used to specifically recognize m6A on mRNA. methylation modified RNA fragments were obtained by immunoprecipitation and used for high-throughput sequencing. By comparing the captured RNA fragments, we found that there were 22381 difference peaks between GR overexpression group and control group, among which 3659 binding peaks were significantly different.Further analysis the MeRIP sequencing results of MIN6 cells overexpressing GR revealed that decreased m6A was detected in a large number of autophagy-related mRNAs.
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Project description:Overexpression of the epidermal growth factor receptor family member Her-2/neu in breast cancer leads to autophosphorylation of the receptor, and induction of multiple downstream signaling pathways including Akt kinase to NF-ï«B cascade that is associated with poor prognosis. Previously, we demonstrated green tea polyhenol epigallocatechin 3-gallate (EGCG) inhibits growth of NF639 Her-2/neu-driven breast cancer cells via reducing receptor autophosphorylation, and downstream Akt and NF-ï«B activities (Pianetti et al., 2002). Interestingly, we noted that upon prolonged culture in the presence of EGCG some cells developed resistance to the polyphenol. Here we report that resistant cells have lost tyrosine phosphorylation on the Her-2/neu receptor. Surprisingly, they displayed elevated NF-ï«B activity, and inhibition of this activity sensitized cells to EGCG. Data from microarray analysis of the original and resistant NF639 populations of cells were subjected to Gene Set Enrichment Analysis (GSEA) pathway analysis, which revealed that the mitogen activated protein kinase (MAPK) pathway was activated in the resistant cells. Treatment of the resistant cells with a combination of EGCG and the MAPK inhibitor U0216 dramatically reduced colony growth and mesenchymal phenotype. Thus, activation of the MAPK pathway mediates resistance to EGCG. Our studies suggest that gene expression profiling of drug resistant cells may provide a mechanism of determining effective systemic therapies for treatment of these advanced cancers. Experiment Overall Design: Total RNA from original NF639 cells and EGCG resistant NF639 cells were harvested using the UltraspecII RNA isolation kit (Biotecx), following the manufacturerâs instruction. The RNA samples were submitted to Boston University Microarray Resource for microarray hybridization using Affymetrix Mouse 430A 2.0 chips. RNAs from two independent experiments were analyzed and data pooled for computational analysis.
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Project description:In the current study, we investigated the modulatory effect of epigallocatechin gallate (EGCG, an active derivative of green tea) on cellular miRNA expression and cell cycle proliferation in NSCLCs (A549). As the IC50 value of EGCG is approximately 304 μM, our studies support the resistance of A549 lung cancer cell by EGCG. In addition, it was interesting to observe its G0/G1 cell cycle arrest activity at 40μM EGCG treatment. So, in the present study, next-generation sequencing (NGS) was used to study the miRNA expression between the cancer control and EGCG-treated samples. A549 cells were treated with 40 μM and 100 μM EGCG. NGS was employed to study the differential expression of novel and known miRNAs. The data generated was analysed with computational approach to study and correlate the expression profiles of both known and novel miRNAs. Differential expression of known miRNAs was observed between control and EGCG-treated samples. Some putative novel miRNA sequences were also observed in the current study. The differential expression levels of putative novel miRNA sequences were estimated by counting the number of reads in the given dataset. Together the analysis of these miRNA profiles revealed log2-fold modulation in the expression levels. We detected 344, 337, and 346 number of known mature miRNAs in control, 40 μM EGCG treated, and 100 μM EGCG treated samples, respectively. We also reported 119, 126, and 125 number of putative novel mature miRNA sequences in control, 40 μM EGCG treated, and 100 μM EGCG treated samples, respectively. In conclusion, the analysis demonstrates that EGCG is actively involved in miRNA modulation in NSCLCs, which further attests to its chemoprotective role and could play a major role in therapeutic applications.
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