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The E2F4/p130 repressor complex cooperates with oncogenic DNp73a to promote cell survival

ABSTRACT: The E2F4/p130 repressor complex cooperates with oncogenic DNp73a to promote cell survival

PROVIDER: PRJNA683078 | ENA |

REPOSITORIES: ENA

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The E2F4/p130 repressor complex cooperates with oncogenic Np73 to promote cell survival

Project description:Tumor suppressor p53 and its related proteins, p63 and p73, can be synthesized as multiple isoforms lacking part of the N- or C-terminal regions. Specifically, high expression of the Np73 isoform is notoriously associated with poor prognosis in cancer. Here, we have performed proteomics analysis of Np73 using as a cellular model human papillomavirus type 38-transformed keratinocytes (38HK) that express high levels of this isoform. We find that Np73 associates with the E2F4/p130 repressor complex through a direct interaction with E2F4. Remarkably, this interaction is favored by the N-terminal truncation of p73 characteristic of Np73 isoforms and is independent of the C-terminal splicing status. We show that the Np73-E2F4/p130 complex is recruited to the promoters of specific genes, thereby enforcing inhibition of their expression both in 38HK and in cancer-derived cell lines. Consistently, silencing of E2F4 in 38HK and in cancer cells resulted in induction of senescence. In conclusion, we have identified and characterized a novel transcriptional regulatory complex that exerts pro-proliferative functions in transformed cells

2023-02-28 | PXD022947 | Pride

The E2F4/p130 repressor complex cooperates with oncogenic ΔNp73α to promote cell survival in human papillomavirus 38 E6/E7-transformed keratinocytes and in cancer cells

Project description:Tumor suppressor p53 and its related proteins, p63 and p73, can be synthesized as multiple isoforms lacking part of the N- or C-terminal regions. Specifically, high expression of the ΔNp73α isoform is notoriously associated with various human malignancies characterized by poor prognosis. This isoform is also accumulated by oncogenic viruses such as Epstein–Barr virus (EBV), as well as genus beta human papillomaviruses (HPV) that appear to be involved in carcinogenesis. To gain additional insight into ΔNp73α mechanisms, we have performed proteomics analyses using human keratinocytes transformed by the E6 and E7 proteins of the beta-HPV type 38 virus as an experimental model (38HK). We find that ΔNp73α associates with the E2F4/p130 repressor complex through a direct interaction with E2F4. This interaction is favored by the N-terminal truncation of p73 characteristic of ΔNp73 isoforms. Moreover, it is independent of the C-terminal splicing status, suggesting that it could represent a general feature of ΔNp73α isoforms (α, β, γ, δ, ε, ζ, θ, η, and η1). We show that the ΔNp73α-E2F4/p130 complex inhibits the expression of specific genes, including genes encoding for negative regulators of proliferation, both in 38HK and in HPV-negative cancer-derived cell lines. Such genes are not inhibited by E2F4/p130 in primary keratinocytes lacking ΔNp73α, indicating that the interaction with ΔNp73α rewires the E2F4 transcriptional program. In conclusion, we have identified and characterized a novel transcriptional regulatory complex with potential implications in oncogenesis.

2021-06-08 | GSE162816 | GEO

Ephexin1 cooperates with K-Ras to promote oncogenic Ras-driven tumorigenesis

Project description:Ephexin1 was initially identified as a neuronal guanine nucleotide exchange factor involved in the control of neuronal development and synaptic homeostasis. Here, we demonstrate that the induction of Ephexin1 expression by an oncogenic K-Ras mutation amplifies the MAPK signaling via direct interaction with oncogenic Ras and contributes to colon and lung tumorigenesis. Ephexin1 cooperates with mutant Ras to accelerate skin tumorigenesis in vivo. In addition, we have demonstrated that the functionally relevant interaction between oncogenic K-Ras and Ephexin1. Together, these findings suggest that Ephexin1 serves as a positive regulator of Ras-driven oncogenesis and potentially represents a novel target for therapeutic intervention.

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Ephexin1 cooperates with K-Ras to promote oncogenic Ras-driven tumorigenesis

Project description:Ephexin1 cooperates with K-Ras to promote oncogenic Ras-driven tumorigenesis

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Mutant p53 cooperates with ETS2 to promote etoposide resistance

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2012-05-02 | E-GEOD-36752 | biostudies-arrayexpress

ChIP-chip analysis of human DREAM complex subunits in G0-arrested and S-phase synchronized cells

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TASOR epigenetic repressor cooperates with a CNOT1 RNA degradation pathway to repress HIV

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Centrosomal kinase Nek2 cooperates with oncogenic pathways to promote metastasis.

Project description: Not available

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Mig-6 deficiency cooperates with oncogenic Kras to promote mouse lung tumorigenesis.

Project description: Not available

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E2F4 and Myc ChIP-chip perfomed on Nimblegen hg17 ENCODE arrays

Project description:Identifying the chromosomal targets of transcription factors is important for reconstructing the transcriptional regulatory networks underlying global gene expression programs. ChIP-chip is a powerful technique to map chromosomal targets of transcription factors. We applied ChIP-chip to map downstream targets of the transcription factor E2F4 and c-Myc. E2F4 is a member of the E2F family of transcriptional regulators that functions as a repressor in quiescent and early G1 cells. c-Myc is a oncogenic transcription factor implicated in almost all aspects of tumorigenesis. We mapped E2F4 and c-Myc binding sites in 1% of the human genome using Nimblegen hg17 ENCODE arrays. Keywords: ChIP-chip

2007-01-20 | GSE6375 | GEO

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