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Transcriptional profile of NOMO1 knockout cell lines

ABSTRACT: Transcriptional profile of NOMO1 knockout cell lines

PROVIDER: PRJNA814734 | 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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Analysis of of the ole of NOMO1 in early-onset colorectal cancer (EOCRC)

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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