The developing role of receptors and adaptors

Massie, Charles E.; Mills, Ian G.

doi:10.1038/nrc1882

Cited by 68 publications

(49 citation statements)

References 65 publications

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“…Following activation, the ligand-receptor complexes are internalized and then enter endosomes, where the receptors and their ligands are sorted to various intracellular destinations (14). Thus, some receptors can be recycled back to the cell surface via early endosomes, and others are targeted to late endosomes and lysosomes for proteolytic degradation.…”

Section: Members Of the Egf Receptor (Egfr)mentioning

confidence: 99%

Ultraviolet Irradiation Can Induce Evasion of Colon Cancer Cells from Stimulation of Epidermal Growth Factor

Adachi

Yasuda

Nakashima

et al. 2011

Journal of Biological Chemistry

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Receptor down-regulation is the most prominent regulatory system of EGF receptor (EGFR) signal attenuation and a critical target for therapy against colon cancer, which is highly dependent on the function of the EGFR. In this study, we investigated the effect of ultraviolet-C (UV-C) on down-regulation of EGFR in human colon cancer cells (SW480, HT29, and DLD-1). UV-C caused inhibition of cell survival and proliferation, concurrently inducing the decrease in cell surface EGFR and subsequently its degradation. UV-C, as well as EGFR kinase inhibitors, decreased the expression level of cyclin D1 and the phosphorylated level of retinoblastoma, indicating that EGFR down-regulation is correlated to cell cycle arrest. Although UV-C caused a marked phosphorylation of EGFR at Ser-1046/1047, UV-C also induced activation of p38 MAPK, a stress-inducible kinase believed to negatively regulate tumorigenesis, and the inhibition of p38 MAPK canceled EGFR phosphorylation at Ser-1046/1047, as well as subsequent internalization and degradation, suggesting that p38 MAPK mediates EGFR down-regulation by UV-C. In addition, phosphorylation of p38 MAPK induced by UV-C was mediated through transforming growth factor-␤-activated kinase-1. Moreover, pretreatment of the cells with UV-C suppressed EGF-induced phosphorylation of EGFR at tyrosine residues in addition to cell survival signal, Akt. Together, these results suggest that UV-C irradiation induces the removal of EGFRs from the cell surface that can protect colon cancer cells from oncogenic stimulation of EGF, resulting in cell cycle arrest. Hence, UV-C might be applied for clinical strategy against human colon cancers. Members of the EGF receptor (EGFR)2 family, which are frequently overexpressed in several types of human cancers, including cancers of the lung (1), head and neck (2), prostate (3), breast (4), pancreas (5), and colon (6), have been associated with abnormal growth of these tumors. It is well known that exposure of cells to EGF results in rapid autophosphorylation of EGFR molecules at the cell surface (7-10), which upon activation lead to cell proliferation, motility, and enhanced survival (11). There are several mechanisms by which EGFR becomes oncogenic including: 1) increased EGFR expression levels, 2) autocrine and/or paracrine growth factor loops, 3) heterodimerization with other EGFR family members and crosstalk with heterologous receptor systems, 4) defective receptor down-regulation, and 5) activating mutations (12). In clinical trials, increasing evidence shows the efficacy of EGFR-targeted agents, including monoclonal antibodies on the one hand and tyrosine kinase inhibitors on the other (13).Following activation, the ligand-receptor complexes are internalized and then enter endosomes, where the receptors and their ligands are sorted to various intracellular destinations (14). Thus, some receptors can be recycled back to the cell surface via early endosomes, and others are targeted to late endosomes and lysosomes for proteolytic degradation. There is increasin...

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Section: Members Of the Egf Receptor (Egfr)mentioning

confidence: 99%

Ultraviolet Irradiation Can Induce Evasion of Colon Cancer Cells from Stimulation of Epidermal Growth Factor

Adachi

Yasuda

Nakashima

et al. 2011

Journal of Biological Chemistry

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“…3A, lanes [5][6][7][8] and the nuclear marker lamin B in the non-nuclear fraction (Fig. 3A, lanes 1-4).…”

Section: Egf-dependent Nuclear Transport Of Egfr Involvesmentioning

confidence: 99%

“…One gradually discovered example of MRIN RTKs, the nuclear EGF receptor (EGFR) family, is involved in multiple cellular functions, including transcriptional regulation, cell proliferation, DNA repair, and chemoand radio-resistance (2)(3)(4)(5)(6)(7)(8)(9)(10). Nuclear EGFR has also been shown to associate with poor prognosis in several cancer types, such as breast cancer, ovarian cancer, and oropharyngeal and esophageal squamous cell carcinomas (11)(12)(13)(14)(15)(16).…”

mentioning

confidence: 99%

Membrane-bound Trafficking Regulates Nuclear Transport of Integral Epidermal Growth Factor Receptor (EGFR) and ErbB-2

Wang

Lee

et al. 2012

Journal of Biological Chemistry

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Background: EGFR is translocated to the inner nuclear membrane through the INTERNET (integral trafficking from the ER to the nuclear envelope transport) pathway. Results: INTERNET regulates EGFR and ErbB-2 but not FGFR-1. Conclusion: At least two different pathways of nuclear transport exist for cell surface receptors.Significance: This provides a new direction for investigating the trafficking mechanisms of various nuclear RTKs.

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“…9,55 Membrane-associated receptors and integrins are numerous, and their role in hematopoiesis is a field of investigation under constant flux that has regularly been reviewed in detail. 51,[56][57][58][59][60][61][62][63][64][65][66][67][68][69][70] We will briefly highlight major points of interest for several of the most studied receptors below and in Table 1.…”

Section: Regulation Of Expression Via Cell Membrane Proteinsmentioning

confidence: 99%

Gene expression changes in normal haematopoietic cells

Lionberger¹,

Stirewalt²

2009

Best Practice & Research Clinical Haematology

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The complexity of the healthy hematopoietic system is immense, and as such, one must understand the biology driving normal hematopoietic expression profiles when designing experiments and interpreting expression data that involves normal cells. This chapter seeks to present an organized approach to the use and interpretation of gene profiling in normal hematopoiesis and broadly illustrates the challenges of selecting appropriate controls for high-throughput expression studies.

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The developing role of receptors and adaptors

Cited by 68 publications

References 65 publications

Ultraviolet Irradiation Can Induce Evasion of Colon Cancer Cells from Stimulation of Epidermal Growth Factor

Ultraviolet Irradiation Can Induce Evasion of Colon Cancer Cells from Stimulation of Epidermal Growth Factor

Membrane-bound Trafficking Regulates Nuclear Transport of Integral Epidermal Growth Factor Receptor (EGFR) and ErbB-2

Gene expression changes in normal haematopoietic cells

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