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A dual-specific IGF-I/II human engineered antibody domain inhibits IGF signaling in breast cancer cells

  1. Author:
    Chen, Zhizhen
    Liu, Jie
    Chu, Dafeng
    Shan, Yaming
    Ma, Guixing
    Zhang, Hongmin
    Zhang, Xiaohua Douglas
    Wang, Pu
    Chen, Qiang
    Deng, Chuxia
    Chen, Weizao
    Dimitrov, Dimiter S.
    Zhao, Qi

  2. Author Address

    Univ Macau, Fac Hlth Sci, Macau, Peoples R China.Univ Calif Los Angeles, Dept Bioengn, Los Angeles, CA USA.Jilin Univ, Sch Life Sci, Natl Engn Lab AIDS Vaccine, Changchun, Jilin, Peoples R China.Southern Univ Sci & Technol, Dept Biol, Guangdong Prov Key Lab Cell Microenvironm & Dis R, Shenzhen Key Lab Cell Microenvironm,SUSTech HKU J, Shenzhen, Guangdong, Peoples R China.Chinese Acad Sci, Shenzhen Inst Adv Technol, Shenzhen, Guangdong, Peoples R China.NCI, Ctr Canc Res, NIH, Frederick, MD 21701 USA.Univ Pittsburgh, Med Sch, Ctr Antibody Therapeut, Pittsburgh, PA 15260 USA.
    1. Year: 2018
    2. Date: May 21
    3. Epub Date: 2018 05 21
  2. Journal: International Journal of Biological Sciences
  3. IVYSPRING INT PUBL,
    1. 14
    2. 7
    3. Pages: 799-806
  5. Type of Article: Article
  6. ISSN: 1449-2288
  1. Abstract:

    The insulin-like growth factors (IGFs), IGF-I and IGF-II, are essential for regulating cell growth, differentiation and metastasis of a broad range of malignancies. The IGF-I/II actions are mediated through the IGF receptor type 1 (IGF-1R) and the insulin receptor (IR), which are overexpressed in multiple types of tumors. Here, we have firstly identified a human engineered antibody domain (eAd) from a phage-displayed VH library. The eAd suppressed the signal transduction of IGF-1R mediated by exogenous IGF-I or IGF-II in breast cancer cell lines through neutralizing both IGF-I and IGF-II. It also significantly inhibited the growth of breast cancer cells. Therefore, the anti-IGF-I/II eAd offers an alternative approach to target both the IGF-1R signaling pathways through the inhibition of IGF-I/II.

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External Sources

  1. View Full Text
  2. DOI: 10.7150/ijbs.25928
  3. PMID: 29910690
  4. PMCID: PMC6001679
  5. View record in Web of Science®
  6. WOS: 000433261800011

Library Notes

  1. Fiscal Year: FY2017-2018
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