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HaCaT cells treated with bleogen pB1 or eGF

ABSTRACT: HaCaT cells treated with bleogen pB1 or eGF

PROVIDER: PRJNA836415 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19142000.fastq.gz	Fastqsanger.gz
	SRR19142001.fastq.gz	Fastqsanger.gz
	SRR19142002.fastq.gz	Fastqsanger.gz
	SRR19142003.fastq.gz	Fastqsanger.gz
	SRR19141995.fastq.gz	Fastqsanger.gz

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HaCaT cells treated with bleogen pB1 or eGF

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Expression data from BCL-3 overexpression HaCat cells

Project description:Constitutive activation of EGFR- and NF-kB-dependent pathways is a hallmark of cancer, yet signaling proteins that connect both oncogenic cascades are poorly characterized. Here we define KIAA1199 as a BCL-3- and p65-dependent gene in transformed keratinocytes. KIAA1199 expression is enhanced upon human papillomavirus (HPV) infection and is aberrantly expressed in clinical cases of cervical (pre)neoplastic lesions. Mechanistically, KIAA1199 binds Plexin A2 and protects from Semaphorin 3A-mediated cell death by promoting EGFR stability and signaling. Moreover, KIAA1199 is an EGFR-binding protein and KIAA1199 deficiency impairs EGF-dependent Src, MEK1 and ERK1/2 phosphorylations. Therefore, EGFR stability and signaling to downstream kinases requires KIAA1199. As such, KIAA1199 promotes EGF-mediated epithelial-mesenchymal transition (EMT). Taken together, our data define KIAA1199 as an oncogenic protein induced by HPV infection and constitutive NF-kB activity that transmits pro-survival and invasive signals through EGFR signaling. We used microarrays to detail the global programme of gene expression upon BCL-3 overexpression We used two experimental conditions, namely HaCat cells infected with a control lentivirus as well as HaCat cells infected with a BCL-3 expressing construct. Both experimental conditions were in triplicates.

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