ArticleMolecular biology of the cell2001
Mechanism in the sequential control of cell morphology and S phase entry by epidermal growth factor involves distinct MEK/ERK activations.
Article in Molecular biology of the cell, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 78 citations in OpenAlex.
- Article
- Chemical screening identifies the anticancer properties ofJournal of Cancer · 2023Article
- Remodeling of the Aged and Emphysematous Lungs: Roles of Microenvironmental Cues.Comprehensive Physiology · 2022Article
- Post-hepatectomy liver regeneration in the context of bile acid homeostasis and the gut-liver signaling axis.Journal of clinical and translational research · 2018Article
- Proliferation and survival of human amniotic epithelial cells during their hepatic differentiation.PloS one · 2018Article
- P2Y2 purinergic receptor activation is essential for efficient hepatocyte proliferation in response to partial hepatectomy.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
- Glucocorticoid-induced suppression of β-cell proliferation is mediated by Mig6.Endocrinology · 2013Article
- Extracellular matrix collagen alters cell proliferation and cell cycle progression of human uterine leiomyoma smooth muscle cells.PloS one · 2013Article
- The MAPK MEK1/2-ERK1/2 Pathway and Its Implication in Hepatocyte Cell Cycle Control.International journal of hepatology · 2012Article
- Eight paths of ERK1/2 signalling pathway regulating hepatocyte proliferation in rat liver regeneration.Journal of genetics · 2011Article
- Inactivation of p38 MAPK during liver regeneration.The international journal of biochemistry & cell biology · 2011Article
- Recombinant human midkine stimulates proliferation of articular chondrocytes.Cell proliferation · 2010Article
- Article
- Cultured rat hepatocytes upregulate Akt and ERK in an ErbB-2-dependent manner.American journal of physiology. Gastrointestinal and liver physiology · 2008Article
- Article
- Inhibition of NF-kappaB activation by the histone deacetylase inhibitor 4-Me2N-BAVAH induces an early G1 cell cycle arrest in primary hepatocytes.Cell proliferation · 2007Article
- Liver stem cells and molecular signaling pathways in hepatocellular carcinoma.Gastrointestinal cancer research : GCR · 2007Article
- Review
- Zonula occludens-1 (ZO-1) redistribution is involved in the regulation of cell dissociation in pancreatic cancer cells.Digestive diseases and sciences · 2005Article
- Cytoskeleton reorganization mediates alpha6beta1 integrin-associated actions of laminin on proliferation and survival, but not on steroidogenesis of ovine granulosa cells.Reproductive biology and endocrinology : RB&E · 2005Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell shape plays a role in cell growth, differentiation, and death. Herein, we used the hepatocyte, a normal, highly differentiated cell characterized by a long G1 phase, to understand the mechanisms that link cell shape to growth. First, evidence was provided that the mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) cascade is a key transduction pathway controlling the hepatocyte morphology. MEK2/ERK2 activation in early G1 phase did not lead to cell proliferation but induced cell shape spreading and demonstration was provided that this MAPK-dependent spreading was required for reaching G1/S transition and DNA replication. Moreover, epidermal growth factor (EGF) was found to control this morphogenic signal in addition to its mitogenic effect. Thus, blockade of cell spreading by cytochalasin D or PD98059 treatment resulted in inhibition of EGF-dependent DNA replication. Our data led us to assess the first third of G1, is exclusively devoted to the growth factor-dependent morphogenic events, whereas the mitogenic signal occurred at only approximately mid-G1 phase. Moreover, these two growth factor-related sequential signaling events involved successively activation of MEK2-ERK2 and then MEK1/2-ERK1/2 isoforms. In addition, we demonstrated that inhibition of extracellular matrix receptor, such as integrin beta1 subunit, leads to cell arrest in G1, whereas EGF was found to up-regulated integrin beta1 and fibronectin in a MEK-ERK-dependent manner. This process in relation to cytoskeletal reorganization could induce hepatocyte spreading, making them permissive for DNA replication. Our results provide new insight into the mechanisms by which a growth factor can temporally control dual morphogenic and mitogenic signals during the G1 phase.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.