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Transcriptional profile of NOMO1 knockout cell lines [RNA-seq]

ABSTRACT: Transcriptional profile of NOMO1 knockout cell lines [RNA-seq]

PROVIDER: PRJNA814735 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18294374_1.fastq.gz	Fastqsanger.gz
	SRR18294374_2.fastq.gz	Fastqsanger.gz
	SRR18294375_1.fastq.gz	Fastqsanger.gz
	SRR18294375_2.fastq.gz	Fastqsanger.gz
	SRR18294376_1.fastq.gz	Fastqsanger.gz

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Transcriptional profile of NOMO1 knockout cell lines

Project description:Transcriptional profile of NOMO1 knockout cell lines

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Transcriptional profile of NOMO1 knockout cell lines [RNA-seq]

Project description:We report the data of high-troughput RNA sequencing of two different cell lines, HCT-116 (early-onset colorectal cancer; EOCRC) and HS-5 (bone marrow) in order to analyze the transcriptional profile generated after NOMO1 (Nodal Modulator 1) gene inactivation, a candidate biomarker in EOCRC. The generation of the NOMO1 knockout cell lines was performed using CRISPR/cas9 technology. The main objective was to identify whether the loss of NOMO1 generated a differential transcriptional profile in each cell line and whether it was possible to identify genes commonly deregulated in the two NOMO1-KO cell lines. RNA sequencing revealed a set of 592 differentially expressed genes (FDR<0.05) in common to the two cell lines as a consequence of NOMO1 inactivation.

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Transcriptional profile of NOMO1 knockout cell lines [Affymetrix]

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Transcriptional profile of NOMO1 knockout cell lines [Affymetrix]

Project description:We report the data of whole Gene expression of three different cell lines, HT-29 (early-onset colorectal cancer, EOCRC), HCT-116 (EOCRC) and HS-5 (bone marrow) in order to analyze the transcriptional profile generated after NOMO1 (Nodal Modulator 1) gene inactivation, a candidate biomarker in EOCRC. The generation of the NOMO1 knockout cell lines was performed using CRISPR/cas9 technology. The main objective was to identify whether the loss of NOMO1 generated a differential transcriptional profile in each cell line and whether it was possible to identify genes commonly deregulated in the three NOMO1-KO cell lines. The analysis revealed a set of differentially expressed genes in common to the three cell lines as a consequence of NOMO1 inactivation.

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Project description:Early-onset colorectal cancer (EOCRC; age younger than 50 years) incidence has been steadily increasing over the last decades worldwide with causes unexplained. A unique molecular feature of EOCRC is that these cases harbor a greater incidence of Nodal Modulator 1 (NOMO1) somatic deletions compared with late-onset CRC. Yet the mechanisms of NOMO1 in early-onset colorectal carcinogenesis are currently unknown. Here we show that 50% of heterozygous NOMO1 deleted–EOCRCs presented pathogenic mutations in this gene, suggesting that NOMO1 can be inactivated by deletion or mutation in EOCRC. To study its role in EOCRC, CRISPR/cas9 technology was used to generate NOMO1 knockout HCT-116 (EOCRC) and HS-5 (bone marrow) cell lines. Loss of NOMO1 in these cell lines did not perturb Nodal pathway signaling. Results from expression microarray, RNA sequencing and protein expression analysis by LC-IMS/MS revealed that NOMO1 inactivation deregulates other signaling pathways independent of the Nodal pathway such as epithelial-mesenchymal transition. Importantly, NOMO1 inactivation increased the migration capacity of CRC cells. Additionally, a gut-specific conditional KO mouse model of NOMO1 revealed no subsequent tumor development in mice. Overall, these findings suggest that NOMO1 could not be a driver of early-onset colorectal carcinogenesis, but its loss promotes an increased migration capacity of CRC cells. Further study is warranted to explore other signaling pathways deregulated by the loss of NOMO1 that may play a relevant role in the pathogenesis of the disease.

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