Auto- and cross-induction within the mammalian epidermal growth factor-related peptide family.

Barnard, J. A.; Graves‐Deal, Ramona; Pittelkow, Mark R.; DuBois, Raymond N.; Cook, Paul W.; Ramsey, G W; Bishop, Phyllis R.; Damstrup, Lars; Coffey, Robert J.

doi:10.1016/s0021-9258(17)31718-0

Cited by 178 publications

(20 citation statements)

References 41 publications

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“…[38][39][40][41][42] In fact, an inhibitor of GGPT I disrupts oncogenic K-Ras processing and signaling. 37 Parental RIE-1 cells, as well as control transfectants and activated Raf-transfected RIE-1 cells, are unaffected by L744,832 treatment, consistent with previous reports showing that normal cells and cells transfected with oncogenes downstream of Ras signaling are resistant to the effects of FTIs. [11][12][13][14][15][16][17][18] The specificity of FTIs for transformed cells is puzzling because Ras function is important in normal mitogenic signaling and is dependent on farnesylation.…”

Section: Discussionsupporting

confidence: 91%

“…Interestingly, pretreatment of parental RIE-1 cells with FTI had no effect on unstimulated proliferation (Figure 1). L744,832 only partially inhibits (20%-30%) TGF-␣-stimulated proliferation and fails to block TGF-␣-stimulated induction of EGF-related peptides in parental RIE-1 cells (Barnard et al 37 and data not shown). The relative inability of FTI to block these events in normal RIE-1 cells suggests that they are mediated by K-Ras signaling or by a Ras-independent pathway.…”

Section: Addition Of Tgf-␣ Overrides Fti Growth Inhibitionmentioning

confidence: 93%

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Pharmacological inhibition of Ras-transformed epithelial cell growth is linked to down-regulation of epidermal growth factor–related peptides

Sizemore¹,

Cox²,

Barnard³

et al. 1999

Gastroenterology

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Section: Discussionsupporting

confidence: 91%

Section: Addition Of Tgf-␣ Overrides Fti Growth Inhibitionmentioning

confidence: 93%

Pharmacological inhibition of Ras-transformed epithelial cell growth is linked to down-regulation of epidermal growth factor–related peptides

Sizemore¹,

Cox²,

Barnard³

et al. 1999

Gastroenterology

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“…Although the long-term effects of continual hepatic EGF production remain unknown, recent studies have shown that EGFR upregulation is common in hepatic carcinogenesis (DeCicco et al 1996(DeCicco et al ,1997 and is frequently observed in carcinomas of the breast and prostate (Glynne-Jones et al 1996;DeJong et al 1998). Because EGF autoregulates the synthesis of its own receptor (Clark et al 1985) and increases expression of other EGFR binding ligands (Barnard et al 1994), such findings support the probability that EGF deregulation constitutes an early upstream event that facilitates growth factor signal amplification and thus contributes to increases in hepatic cell division during the course of chronic toxicity or injury.…”

Section: Discussionmentioning

confidence: 71%

Expression of Epidermal Growth Factor and Its Receptor in Cirrhotic Liver Disease

Kömüves

Feren

Jones

et al. 2000

J Histochem Cytochem.

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Polypeptide growth factors, including epidermal growth factor (EGF), play a central role in regulating hepatocyte growth both in vivo and in primary culture. To characterize EGF gene expression in the pathogenesis of regenerative cirrhotic fibrosis, we employed biotinylated antisense oligonucleotide probes to localize hepatic mRNA transcripts in situ. In control tissue and regenerative hepatic nodules, EGF receptor (EGFR) mRNA transcripts were expressed constitutively. In contrast, oligonucleotide probes targeting the human EGF coding region showed that EGF transcription was extremely low in control liver but was highly elevated and localized to regenerative hepatic nodules and bile duct epithelia of cirrhotic liver. To determine whether EGF mRNA accumulation accompanied a comparable increase in the EGF peptide, we performed immunohistochemistry using an antibody specific for the nonprocessed peptide aminoterminus. We observed that positive localized EGF staining paralleled its mRNA transcript. These results indicate that EGF upregulation is a characteristic of cirrhotic liver disease and suggest that persistent de novo ligand synthesis and its signaling contribute to an autocrine-mediated hepatocyte proliferation within the regenerative nodule.

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“…Previous work (Coffey et al, 1987) identified upregulation of TGF-α mRNA and protein by EGF, and described the phenomenon of autoregulation of TGF-α gene expression in cultured keratinocytes. Other studies (Barnard et al, 1994;Hashimoto et al, 1994) have reported the cross-regulation of EGF-family growth factor gene expression by these same factors in several epithelial cell types, suggesting complexity in the molecular mechanisms that are involved in induction of these factors. Therefore, these growth factors may act not only by autoinduction but also through mutual amplification mechanisms.…”

Section: Discussionmentioning

confidence: 95%

“…These factors display equivalent affinity for EGFR in an intestinal epithelial cell line (Barnard et al, 1994). The EGFR is a 170 kDa transmembrane glycoprotein consisting of an extracellular binding domain and an intracellular domain that exhibits tyrosine kinase activity.…”

mentioning

confidence: 99%

Endogenous EGF-Family Growth Factors are Necessary for the Progression from the G1 to S Phase in Human Keratinocytes

Kobayashi

Hashimoto²,

Okumura³

et al. 1998

Journal of Investigative Dermatology

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Recently several endogenous epidermal growth factor (EGF)-family growth factors (transforming growth factor-alpha, amphiregulin, and heparin-binding EGF-like growth factor) have been identified in human keratinocytes. These factors are known to play an important role in the regulation of cell proliferation. Here we show that the interaction between these factors and EGF receptor are key factors in the progression from the G1 phase to the S phase (the G1/S progression) in human keratinocytes. In this study, human keratinocytes were cultured in serum-free MCDB153 medium and then partially synchronized by isoleucine deprivation. After synchronization, the number of S phase cells increased and reached a maximum after 18-24 h. The immediate addition of anti-EGF receptor blocking antibody (1 microg per ml) to synchronized cells decreased S phase cells by 42.5% compared with untreated keratinocytes at 18 h. By contrast, the addition of anti-EGF receptor antibodies at 12 h or later did not alter the percentage of S phase cells. Northern blot analysis of synchronized cells demonstrated that mRNA expression of transforming growth factor-alpha, amphiregulin, heparin-binding EGF-like growth factor, and EGF receptor reached a maximum within 0.5-3 h after synchronization, when many cells initiated progression from the G1 to the S phase. The results show that anti-EGF receptor antibodies block the G1/S progression and the rapid increase of mRNA expression of endogenous EGF-family growth factors and EGF receptor during G1/S progression. These findings indicate that growth factor binding and EGF receptor activation are involved in the G1/S cell cycle progression of human keratinocytes.

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Auto- and cross-induction within the mammalian epidermal growth factor-related peptide family.

Cited by 178 publications

References 41 publications

Pharmacological inhibition of Ras-transformed epithelial cell growth is linked to down-regulation of epidermal growth factor–related peptides

Pharmacological inhibition of Ras-transformed epithelial cell growth is linked to down-regulation of epidermal growth factor–related peptides

Expression of Epidermal Growth Factor and Its Receptor in Cirrhotic Liver Disease

Endogenous EGF-Family Growth Factors are Necessary for the Progression from the G1 to S Phase in Human Keratinocytes

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