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Endothelin causes transactivation of the EGFR and HER2 in non-small cell lung cancer cells

  1. Author:
    Moody, Terry W.
    Ramos-Alvarez, Irene
    Moreno, Paula
    Mantey, Samuel A.
    Ridnour, Lisa
    Wink, David
    Jensen, Robert T.

  2. Author Address

    NCI, Dept Hlth & Human Serv, Ctr Canc Res, Off Director, Bethesda, MD 20892 USA.NIDDK, NIH, Digest Dis Branch, Bethesda, MD 20892 USA.NCI, Canc Inflammat Program, Frederick, MD 21702 USA.
    1. Year: 2017
    2. Date: Apr
  2. Journal: PEPTIDES
  3. ELSEVIER SCIENCE INC,
    1. 90
    2. Pages: 90-99
  5. Type of Article: Article
  6. ISSN: 0196-9781
  1. Abstract:

    Endothelin (ET)-1 is an important peptide in cancer progression stimulating cellular proliferation, tumor angiogenesis and metastasis. ET-1 binds with high affinity to the ETA receptor (R) and ETBR on cancer cells. High levels of tumor ET-1 and ETAR are associated with poor survival of lung cancer patients. Here the effects of ET-1 on epidermal growth factor (EGF)R and HER2 transactivation were investigated using non small cell lung cancer (NSCLC) cells. ETAR mRNA was present in all 10 NSCLC cell lines examined. Addition of ET-1 to NCI-H838 or H1975 cells increased EGFR, HER2 and ERK tyrosine phosphorylation within 2 min. The increase in EGFR and HER2 transactivation caused by ET-1 addition to NSCLC cells was inhibited by lapatinib (EGFR and HER2 tyrosine kinase inhibitor (TKI)), gefitinib (EGFRTKI), ZD4054 or BQ-123 (ETAR antagonist), GM6001 (matrix metalloprotease inhibitor), PP2 (Src inhibitor) or Tiron (superoxide scavenger). ET-1 addition to NSCLC cells increased cytosolic Ca2+ and reactive oxygen species. ET-1 increased NSCLC clonal growth, whereas BQ123, ZD4054, lapatinib or gefitinib inhibited proliferation. The results indicate that ET-1 may regulate NSCLC cellular proliferation in an EGFR- and HER2-dependent manner. Published by Elsevier Inc.

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External Sources

  1. View Full Text
  2. DOI: 10.1016/j.peptides.2017.01.012
  3. PMID: 28153500
  4. PMCID: PMC5421360
  5. View record in Web of Science®
  6. WOS: 000399516300013

Library Notes

  1. Fiscal Year: FY2016-2017
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