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Related Experiment Videos

Growth factors modify the epidermal growth factor receptor through multiple pathways.

B A Friedman, M R Rosner

    Journal of Cellular Biochemistry
    |May 1, 1987
    PubMed
    Summary

    Tumor promoters alter epidermal growth factor (EGF) receptor properties via protein kinase C. This study reveals two factors in v-sis transformed cells affecting EGF binding, one dependent and one independent of protein kinase C.

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    Area of Science:

    • Cell Biology
    • Molecular Oncology
    • Signal Transduction

    Background:

    • Tumor promoters modulate epidermal growth factor (EGF) receptor activity through protein kinase C (PKC) activation.
    • Platelet-derived growth factor (PDGF) and p28sis are diacylglycerol-generating factors expected to activate PKC and influence EGF receptor properties.

    Purpose of the Study:

    • To investigate the direct involvement of PKC in the effects of v-sis-transformed cell media on the EGF receptor.
    • To differentiate between PKC-dependent and -independent mechanisms regulating EGF receptor function.

    Main Methods:

    • Swiss 3T3 cells were pre-treated with phorbol dibutyrate (PDBu) to reduce active PKC levels, assessing subsequent responsiveness.
    • Analysis of EGF receptor binding properties in response to media from v-sis-transformed cells under varying conditions.

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    Main Results:

    • Media from v-sis-transformed cells exhibit two components affecting EGF binding: a PKC-independent labile factor and a PKC-dependent stable factor.
    • The PKC-independent factor's action was not mimicked by TGF-β or EGF, with or without PDGF.
    • The PKC-dependent factor's action resembled that of PDGF.

    Conclusions:

    • Heterologous regulation of the EGF receptor involves both PKC-dependent and PKC-independent signaling pathways.
    • V-sis-transformed cells release factors that differentially modulate EGF receptor activity through distinct mechanisms.