Arca subcrenata Polypeptides Inhibit Human Colorectal Cancer HT-29 Cells Growth via Suppression of IGF-1R/Akt/mTOR Signaling and ATP Production

Nutr Cancer. 2020;72(2):260-272. doi: 10.1080/01635581.2019.1625935. Epub 2019 Jul 11.

Abstract

Arca subcrenata Lischke, widely scattering offshore at neritic regions, is very popular on dining table due to its edible and medical functional meatball. This study aims to investigate the suppression of a polypeptide fraction from A. subcrenata (PAS) on human colorectal cancer HT-29 cells, and its underlying mechanism. The results showed that PAS inhibited the growth of HT-29 cells with an IC50 value of 117 μg/ml after 48 h treatment, and significantly suppressed the tumor growth in nude mice bearing-xenografted HT-29 cells at the dosage of 63 mg/kg, with little influence on normal colon cells and normal colonic mucosa. PAS was then inspiringly found to induce apoptosis and G2/M phase arrest in HT-29 cells. The effect mechanism was involved in the inhibition of IGF-1/IGF-1R signaling activation, which was responsible for inactivating downstream Akt/mTOR pathway. Immunofluorescence assay also showed that PAS could reduce phosphorylation of IGF-1R (Tyr1165/1166). IGF-1, an IGF-1R activator, could reverse the suppression of PAS on IGF-1R phosphorylation. Furthermore, PAS significantly inhibited ATP production of HT-29 cells both in vitro and in vivo. Our results provide positive evidence that A. subcrenata has the potential to be a candidate for the treatment of colorectal cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Triphosphate / biosynthesis*
  • Animals
  • Apoptosis
  • Arcidae / chemistry*
  • Cell Line, Tumor
  • Cell Proliferation
  • Colorectal Neoplasms / drug therapy*
  • Colorectal Neoplasms / metabolism
  • Colorectal Neoplasms / pathology
  • HT29 Cells
  • Humans
  • Male
  • Mice
  • Mice, Nude
  • Peptides / pharmacology*
  • Phosphorylation
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Receptor, IGF Type 1 / metabolism*
  • Signal Transduction
  • TOR Serine-Threonine Kinases / metabolism*
  • Xenograft Model Antitumor Assays

Substances

  • IGF1R protein, human
  • Peptides
  • Adenosine Triphosphate
  • MTOR protein, human
  • Receptor, IGF Type 1
  • AKT1 protein, human
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases