A Historical Perspective of the EGF Receptor and Related Systems

Edwin, Francis; Wiepz, Gregory J.; Singh, Rakesh K.; Peet, Chimera R.; Chaturvedi, Deepti; Bertics, Paul J.; Patel, Tarun B.

doi:10.1385/1-59745-012-x:1

Cited by 41 publications

(40 citation statements)

References 139 publications

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“…Besides activation by its cognate ligand EGF, EGFR has been reported to be transactivated by a considerable number of cell surface molecules to convey growth signals (23). For example, receptors for prolactin, growth hormones, and adhesion molecules as well as stress factors such as oxidants and irradiation are reported to transactivate EGFR.…”

Section: Discussionmentioning

confidence: 99%

Transactivation of the Epidermal Growth Factor Receptor by Formylpeptide Receptor Exacerbates the Malignant Behavior of Human Glioblastoma Cells

Huang

Bian

et al. 2007

Cancer Research

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The G protein-coupled formylpeptide receptor (FPR), which mediates leukocyte migration in response to bacterial and host-derived chemotactic peptides, promotes the chemotaxis, survival, and tumorigenesis of highly malignant human glioblastoma cells. Because glioblastoma cells may also express other receptors for growth signals, such as the epidermal growth factor (EGF) receptor (EGFR), we investigated the role of EGFR in the signaling cascade of FPR and how two receptors cross-talk to exacerbate tumor growth. We found that N-formyl-methionyl-leucyl-phenylalanine, an FPR agonist peptide, rapidly induced EGFR phosphorylation at tyrosine residue (Tyr) 992, but not residues 846, 1068, or 1173, in glioblastoma cells, whereas all these residues were phosphorylated after only EGF treatment. The FPR agonist-induced EGFR phosphorylation in tumor cells was dependent on the presence of FPR as well as GAi proteins, and was controlled by Src tyrosine kinase. The transactivation of EGFR contributes to the biological function of FPR in glioblastoma cells because inhibition of EGFR phosphorylation significantly reduced FPR agonist-induced tumor cell chemotaxis and proliferation. Furthermore, depletion of both FPR and EGFR by short interference RNA abolished the tumorigenesis of the glioblastoma cells. Our study indicates that the glioblastoma-promoting activity of FPR is mediated in part by transactivation of EGFR and the cross-talk between two receptors exacerbates the malignant phenotype of tumor cells. Thus, targeting both receptors may yield antiglioblastoma agents superior to those targeting one of them. [Cancer Res 2007;67(12):5906-13]

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Section: Discussionmentioning

confidence: 99%

Transactivation of the Epidermal Growth Factor Receptor by Formylpeptide Receptor Exacerbates the Malignant Behavior of Human Glioblastoma Cells

Huang

Bian

et al. 2007

Cancer Research

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“…Inhibitors of the extracellular signal-regulated kinases (ERK) slow cyst growth and expansion more dramatically. Both P2Y and P2X receptors can trigger ERK activation [156][157][158], as can growth factor receptors [159]. It is well known that purinergic receptor systems can transactivate growth factor receptor systems and cytokine receptor systems [134,160].…”

Section: Nucleotide and Nucleoside Receptor Expression Along The Nephronmentioning

confidence: 99%

Purinergic signaling in the lumen of a normal nephron and in remodeled PKD encapsulated cysts

Hovater

Olteanu

Welty

et al. 2008

Purinergic Signalling

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The nephron is the functional unit of the kidney. Blood and plasma are continually filtered within the glomeruli that begin each nephron. Adenosine 5′ triphosphate (ATP) and its metabolites are freely filtered by each glomerulus and enter the lumen of each nephron beginning at the proximal convoluted tubule (PCT). Flow rate, osmolality, and other mechanical or chemical stimuli for ATP secretion are present in each nephron segment. These ATP-release stimuli are also different in each nephron segment due to water or salt permeability or impermeability along different luminal membranes of the cells that line each nephron segment. Each of the above stimuli can trigger additional ATP release into the lumen of a nephron segment. Each nephron-lining epithelial cell is a potential source of secreted ATP. Together with filtered ATP and its metabolites derived from the glomerulus, secreted ATP and adenosine derived from cells along the nephron are likely the principal two of several nucleotide and nucleoside candidates for renal autocrine and paracrine ligands within the tubular fluid of the nephron. This minireview discusses the first principles of purinergic signaling as they relate to the nephron and the urinary bladder. The review discusses how the lumen of a renal tubule presents an ideal purinergic signaling microenvironment. The review also illustrates how remodeled and encapsulated cysts in autosomal dominant polycystic kidney disease (ADPKD) and remodeled pseudocysts in autosomal recessive PKD (ARPKD) of the renal collecting duct likely create an even more ideal microenvironment for purinergic signaling. Once trapped in these closed microenvironments, purinergic signaling becomes chronic and likely plays a significant epigenetic and detrimental role in the secondary progression of PKD, once the remodeling of the renal tissue has begun. In PKD cystic microenvironments, we argue that normal purinergic signaling within the lumen of the nephron provides detrimental acceleration of ADPKD once remodeling is complete.

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“…Odgrywają one istotną rolę w wielu procesach fizjologicznych, jak wzrost i implantacja zarodka, biorą udział w procesach naprawczych dojrzałych i uszkodzonych organów (15,65). Nadekspresja EGFR jednak może prowadzić do niekontrolowanego podziału komórek, a w konsekwencji rozwoju nowotworu.…”

Section: Nabłonkowy Czynnik Wzrostu (Epidermal Growth Factor Egf)unclassified

Relevant aspects of the influence of chosen growth factors on the activity of the female reproductive system

Woźna¹,

Rybska²,

Swierczewska³

et al. 2017

Medycyna Weterynaryjna

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*) Projekt został sfinansowany ze środków Narodowego Centrum Nauki przyznanych na podstawie decyzji DEC-2013/09/N/NZ5/0183. Woźna M., Rybska M., Świerczewska M., Jaśkowski J. M.Relevant aspects of the influence of chosen growth factors on the activity of the female reproductive system Summary The endometrium of the uterus is a highly dynamic structure in terms of its changes during the various stages of the sexual cycle. These changes are the result of cyclical fluctuations in the concentrations of steroid hormones and local factors of an auto -and paracrine -nature. This condition indicates that the causes of degenerative processes of the uterus must be sought not only in disorders of the hormonal profile and bacterial infections but also disorders at the molecular level. Factors that may play a key role in the formation and development of various pathologies of the female reproductive system include growth factors and their receptors (growth factors -GFs). Discussing these growth factors in the work may provide useful molecular markers that identify pathological conditions of the endometrium. Subject to expression in the endometrium, they are involved in the regulation of cell proliferation, migration and secretion of the glandular epithelium, they also regulate physiological and pathological angiogenesis, revealing strong pro-inflammatory effects. In this research, the authors present an overview of current scientific reports indicating that changes in the expression of studied factors, and thus disturbances in their effects, may constitute one of the causes of pathogenesis within the uterus in many animal species.

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A Historical Perspective of the EGF Receptor and Related Systems

Cited by 41 publications

References 139 publications

Transactivation of the Epidermal Growth Factor Receptor by Formylpeptide Receptor Exacerbates the Malignant Behavior of Human Glioblastoma Cells

Transactivation of the Epidermal Growth Factor Receptor by Formylpeptide Receptor Exacerbates the Malignant Behavior of Human Glioblastoma Cells

Purinergic signaling in the lumen of a normal nephron and in remodeled PKD encapsulated cysts

Relevant aspects of the influence of chosen growth factors on the activity of the female reproductive system

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