Nuclear expression of E2F4 induces cell death via multiple pathways in normal human intestinal epithelial crypt cells but not in colon cancer cells.

@article{Garneau2007NuclearEO,
  title={Nuclear expression of E2F4 induces cell death via multiple pathways in normal human intestinal epithelial crypt cells but not in colon cancer cells.},
  author={Hugo Garneau and Laetitia Alvarez and Marie-Christine Paquin and Carine R. Lussier and Claudine Rancourt and Eric A Tremblay and Jean-François Beaulieu and Nathalie Rivard},
  journal={American journal of physiology. Gastrointestinal and liver physiology},
  year={2007},
  volume={293 4},
  pages={
          G758-72
        }
}
E2F transcription factors control cell cycle progression. The localization of E2F4 in intestinal epithelial cells is cell cycle dependent, being cytoplasmic in quiescent differentiated cells but nuclear in proliferative cells. However, whether nuclear translocation of E2F4 alone is sufficient to trigger intestinal epithelial cell proliferation remains to be established. Adenoviruses expressing fusion proteins between green fluorescent protein (GFP) and wild-type (wt)E2F4 or GFP and nuclear… 
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E2F4 expression is required for cell cycle progression of normal intestinal crypt cells and colorectal cancer cells
TLDR
It is demonstrated that lentiviral infection of an shRNA which specifically knocked‐down E2F4 expression slowed down G1/S phase transition and the proliferation rate of normal human intestinal epithelial cells (HIEC) and of colon cancer cells, and indicates that nuclear E 2F4 may be determinant in the promotion of proliferation of human intestine epithelial crypt cells and colorectal cancer cells.
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The results point to a possible direct tumor-promoting role for E2F4 in the context of colorectal carcinogenesis, and the inverse immunohistochemical relationship between E 2F1 and E2f4 indicates a possible mechanistic interlink in coloreCTal cancer.
E2F transcription factors and digestive system malignancies: how much do we know?
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It appears that targeted approaches using E2F-agonists or antagonists should take into account the tissue-dependent function of each E1F member, to clarify their role in carcinogenesis.
Interplay between NRF1, E2F4 and MYC transcription factors regulating common target genes contributes to cancer development and progression
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NRF1 may orchestrate both MYC and E2F4 to regulate common target genes linked to multiple networks in the development and progression of cancer, setting the stage for the design of novel treatment strategies.
15‐lipoxygenase‐1 exerts its tumor suppressive role by inhibiting nuclear factor‐kappa B via activation of PPAR gamma
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It is shown that ectopic expression of 15‐LOX‐1 gene in HCT‐116 and HT‐29 CRC cell lines inhibited the degradation of inhibitor of kappa B (IκBα), decreased nuclear translocation of p65 and p50, decreased DNA binding in the nucleus and decreased transcriptional activity of Nuclear factor kappaB (NF‐κB).
In Silico Discovery of Mitosis Regulation Networks Associated with Early Distant Metastases in Estrogen Receptor Positive Breast Cancers
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A subset of 44 differently expressed genes (DEGs) was found common to all three studies and characterized by mitotic checkpoint genes and pathways that regulate mitotic spindle and chromosome dynamics, which may reflect the clinical utility of mitotic poisons in metastatic breast cancer.
Isolation, characterization, and culture of normal human intestinal crypt and villus cells.
TLDR
In the laboratory, using fetal human intestines obtained at mid-gestation, the first normal human intestinal epithelial crypt-like (HIEC) cell line and villus-like primary cultures of differentiated enterocytes (PCDE) are generated.
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