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KMT9 controls growth and stemness of colorectal cancer

ABSTRACT: KMT9 controls growth and stemness of colorectal cancer

PROVIDER: PRJNA632605 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11786400_1.fastq.gz	Fastqsanger.gz
	SRR11786400_2.fastq.gz	Fastqsanger.gz
	SRR11786401_1.fastq.gz	Fastqsanger.gz
	SRR11786401_2.fastq.gz	Fastqsanger.gz
	SRR11786402_1.fastq.gz	Fastqsanger.gz

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Project description:The unfolded protein response (UPR) maintains endoplasmic reticulum (ER) homeostasis by sensing protein-folding stress and orchestrating cellular adaptation via the ER-transmembrane proteins IRE1, PERK and ATF6. Malignant cells can co-opt UPR signaling by IRE1 and PERK to sustain tumor growth; however, the importance of ATF6 in cancer remains poorly deciphered. We observed elevated ATF6 transcriptional activity in several cancers including colorectal carcinoma (CRC). Genetic silencing or small molecule inhibition of ATF6 blocked cell cycle progression and reduced viability of several human CRC cell lines in vitro and disrupted tumor progression in vivo. Unexpectedly, ATF6 interference also disabled Myc and Wnt signaling and reduced stemness. ATF6 inhibition attenuated growth of organoids derived from malignant but not normal human intestinal tissue, reducing Wnt-pathway activity and driving cellular differentiation. Wnt-surrogate agonism rescued the growth inhibitory phenotype of ATF6 interference. Our findings identify ATF6 as an unexpected facilitator of oncogenic Wnt signaling in CRC.

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KMT9 is an actionable target in muscle-invasive bladder cancer

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