Human IGF-I Eb-peptide induces cell attachment and lamellipodia outspread of metastatic breast carcinoma cells (MDA-MB-231)

Exp Cell Res. 2017 Sep 15;358(2):199-208. doi: 10.1016/j.yexcr.2017.06.015. Epub 2017 Jun 27.

Abstract

Although Insulin-like growth factor (IGF-I) has been intensively studied, the functions of E-domain peptides of pro-IGF-I, however, have been overlooked. In our laboratory, several anti-cancer activities of the E-peptide of pro-IGF-I have been identified for the longest isoforms of human and rainbow trout E-peptides. These activities include dose-dependent inhibition of colony formation, inhibition of cancer cell metastasis and invasion through matrigel, suppression of cancer-induced angiogenesis, and attenuation of expression of apoptotic genes in favor of cell death. In this study, we were able to produce two-tagged recombinant human Eb-peptide (hEb) of pro-IGF-I with a purity over 99%. With its antimicrobial peptide (AMP)-like characteristics such as binding to the cytoplasmic membrane, and the affinity to the substratum of culture plate, hEb forms a layer of interface rapidly which facilitates the attachment of breast carcinoma cells, MDA-MB-231. Furthermore, the likely conformational change of homo-dimerized hEb through a single disulfide bond, as well as the ability to trigger clathrin-mediated endocytosis may play important roles for inducing lamellipodia outspread in MDA-MB-231 cells. With the highly purified hEb-peptide, not only could we study its function(s) in detail but also the minimum requirement for cancerous cells to metastasize to a suitable environment and grow.

Keywords: Anti-cancer; Antimicrobial peptides (AMPs); Clathrin-mediated endocytosis (CME); Lamellipodia; Metastasis; hEb (human IGF-I E-domain peptide).

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Breast Neoplasms / metabolism*
  • Cell Adhesion
  • Cell Division / physiology
  • Cell Line, Tumor
  • Cell-Matrix Junctions / metabolism*
  • Female
  • Gene Expression Regulation, Neoplastic / genetics*
  • Humans
  • Insulin-Like Growth Factor I / metabolism*
  • Insulin-Like Growth Factor II
  • Peptide Fragments
  • Protein Precursors / metabolism*
  • Pseudopodia / metabolism
  • Recombinant Proteins / metabolism

Substances

  • Peptide Fragments
  • Protein Precursors
  • Recombinant Proteins
  • pro-insulin-like growth factor I
  • proinsulin-like growth factor II (117-156)
  • Insulin-Like Growth Factor I
  • Insulin-Like Growth Factor II