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MiRNA expression profiles of HeLa-Cas9 and NCI-N87 cells

ABSTRACT: miRNA expression profiles of HeLa-Cas9 and NCI-N87 cells

PROVIDER: PRJNA434552 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6748445.fastq.gz	Fastqsanger.gz
	SRR6748446.fastq.gz	Fastqsanger.gz
	SRR6748447.fastq.gz	Fastqsanger.gz
	SRR6748448.fastq.gz	Fastqsanger.gz
	SRR6748449.fastq.gz	Fastqsanger.gz

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miRNA expression profiles of HeLa-Cas9 and NCI-N87 cells

Project description:MicroRNAs (miRNAs) play an important role in the regulation of gene expression and are often dysregulated in disease. The recent development of the CRISPR-Cas9 gene-editing system, composed of the Cas9 nuclease in complex with a single guide RNA (sgRNA), allows researchers to direct DNA cleavage at a predetermined site and to conduct genome-scale knockout screens. To determine the functional role of miRNAs in cancer, we designed and constructed a library of 7,382 sgRNAs to target 85% of the 1,881 annotated human miRNA stem-loops. We then examined the role of miRNAs in HeLa cell fitness by monitoring the change in frequency of each sgRNA over time. We identified 44 pro-proliferative miRNAs from two replicate experiments, including miR-31, a known cervical cancer overexpressing miRNA that enhances HeLa cell proliferation. We also examined the role of miRNAs in NCI-N87 gastric cancer cells and identified 10 pro-fitness and 10 anti-fitness miRNAs. In both screens, many of the pro-fitness miRNAs identified are overexpressed in tumors cervical tumors for HeLa or gastric tumors for NCI-N87. In summary, we present a CRISPR miRNA-targeted screen which was able to identify both known and novel fitness-associated miRNAs in the HeLa and NCI-N87 cell lines.

2018-06-21 | GSE110784 | GEO

ATAC-seq of human gastric adenocarcinoma NCI-N87 cell line treated with lapatinib

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Project description:We compared gene expression profiles in trastuzumab-sensitive NCI-N87 cell line versus four trastuzumab-resistant cell lines (N87-TR1, N87-TR2, N87-TR3, N87-TR4) by microarray analysis in order to identify groups of genes associated with a specific signaling pathway or biological process.

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Project description:To identify ARID1A-regulated genes in stomach cancer, we performed microarray profiling of RNA isolated from N87 stomach cancer cells, in which ARID1A expression was knocked down by two different siRNAs against ARID1A.

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Lacticaseibacillus casei strain:N87

Project description:Lacticaseibacillus casei strain:N87 Genome sequencing and assembly

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Expression data from human cell lines before and after treated with drugs.

Project description:Analysis of HER2-amplified NCI-N87 gastric cancer cell line exposed to 0.1 µg/mL T-DM1 and subsequently cultured in the presence of gradually increasing doses, up to a maximum of 4 µg/mL. The resultant cell lines that grew exponentially in the presence of T-DM1 were designated as drug resistant gastric cancer cell lines, and named N87-TDMR. We used microarrays to detail the gene expression in N87-TDMR and N87-parent cells to screen for transcripts correlated with T-DM1 resistance.

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Project description:Background: Egl-9 family hypoxia inducible factor 3 (EGLN3) belongs to the family of 2-oxoglutarate (2-OG)- and ferrous iron (Fe 2+)-dependent dioxygenases, which play critical roles in all steps of tumorigenesis. Previous studies have found that EGLN3 regulates the malignant biological behavior of malignant tumors. However, its role and mechanism in the occurrence and development of gastric cancer (GC) are still unclear. This study aimed to investigate the role of EGLN3 in gastric carcinogenesis Methods:Bioinformatics analysis, qRT-PCR, western blot, CCK-8, and in vivo xenograft tumor model were used to examine the expression and function of EGLN3. Survival analysis was performed to determine the correlation between EGLN3 expression and prognosis of patients with GC. Genes modulated by EGLN3 in NCI-N87 cells were identified through RNA next generation sequence screening and further verified by qRT-PCR in NCI-N87 cells. Results: EGLN3 expression was markedly reduced in GC tissues as compared with that in normal tissues. Likewise, EGLN3 expression was also significantly reduced in a panel of GC cell lines . Forced expression of EGLN3 inhibited proliferation in NCI-N87 cells in vitro. Additionally, EGLN3 impaired growth of NCI-N87 cells in immunodeficient mice. Survival analysis showed that EGLN3 expression was positively associated with favorable outcome in patients with GC.

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Project description:H1-HeLa cells were stably transduced with lentiCas9-Blast (Addgene, Plasmid #52962) and subsequently selected using blasticidin to generate constitutively expressing Cas9 H1-HeLa cells. A single Cas9-expressing H1-HeLa clone was then transduced with lentivirus without a selection marker to stably express CDHR3 C529Y (H1-HeLa+CDHR3). A single CDHR3-expressing H1-HeLa clone was then chosen based on RT-qPCR of CHDR3 expression and RV-C15 RNA levels for mutagenesis. 300 million of the H1-HeLa cells constitutively expressing CDHR3 and Cas9 were transduced with the lentiGuide-Puro from the GeCKO v2 library at a MOI of 0.3. Cells were selected using puromycin and heterogeneous H1-HeLa knockout cell populations were subsequently pooled together. The CRISPR genetic screens were started 10 days post transduction. >1000-fold coverage of mutagenized cells (libraries A and B) was infected with either RV-C15 (MOI=1 PFU/cell) or EV-D68 Missouri (MOI=1 PFU/cell). RV-C15 infection was repeated for an additional round at 6 days post-infection. As soon as appearance of visibly viable colonies was observed, populations of virus-resistant cells were pooled and harvested. Uninfected starting populations of mutagenized cells were used as the unselected reference. Total genomic DNA from both virus-resistant and uninfected cells was respectively extracted using QIAamp DNA Mini Kit (Qiagen). The inserted guide RNA sequences were retrieved from the genomic DNA by PCR amplification. The PCR products were then purified and subjected to NextSeq platform (Illumina) next-generation sequencing.

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