A tropomyosin-like Meretrix meretrix Linnaeus polypeptide inhibits the proliferation and metastasis of glioma cells via microtubule polymerization and FAK/Akt/MMPs signaling.

Abstract

Glioblastoma (GBM) represents the most common, aggressive and deadliest primary tumors with poor prognosis as available therapeutic approaches fail to control its aberrant proliferation and high invasiveness. Thus, the therapeutic agents targeting these two characteristics will be more effective. In present study, a novel polypeptide (MM15), which was originally purified from Meretrix meretrix Linnaeus and has been proven to possess potent antitumor activity by our laboratory, was recombinant expressed and identified as a tropomyosin homologous protein. The recombinant polypeptide (re-MM15) could induce the U87 cell cycle arrest in G2/M phase and cell apoptosis by inducing tubulin polymerization. Additionally, re-MM15 displayed the significant inhibition to the migration and invasion of U87 cells through downregulating FAK/Akt/MMPs signaling. Furthermore, the in vivo analysis suggested that re-MM15 significantly blocked tumor growth in U87 xenograft model. Collectively, our results indicated that re-MM15, with anti-GBM properties in vitro and in vivo, has promising potential as a new anticancer candidate for GBM.

• Authors: Zhongjun Fan, Qi Xu, Changhui Wang, Xiukun Lin, Quanbin Zhang, Ning Wu
• Journal: International journal of biological macromolecules (Int J Biol Macromol) Vol. 145 Pg. 154-164 (Feb 15 2020) ISSN: 1879-0003 [Electronic] Netherlands
• PMID: 31866539 (Publication Type: Journal Article)
• Copyright: Copyright © 2019 Elsevier B.V. All rights reserved.

Chemical References

• Antineoplastic Agents
• FAK peptide
• Peptides
• Tropomyosin
• Proto-Oncogene Proteins c-akt
• Matrix Metalloproteinases

Topics

• Animals
• Antineoplastic Agents (pharmacology)
• Apoptosis (drug effects)
• Cell Cycle Checkpoints (drug effects)
• Cell Line, Tumor
• Cell Movement (drug effects)
• Cell Proliferation (drug effects)
• Glioblastoma (drug therapy, metabolism)
• Glioma (drug therapy, metabolism)
• HCT116 Cells
• HeLa Cells
• Humans
• MCF-7 Cells
• Matrix Metalloproteinases (metabolism)
• Mice
• Mice, Nude
• Microtubules (metabolism)
• NIH 3T3 Cells
• Peptides (metabolism, pharmacology)
• Polymerization (drug effects)
• Proto-Oncogene Proteins c-akt (metabolism)
• Signal Transduction (drug effects)
• Tropomyosin (pharmacology)
• Xenograft Model Antitumor Assays (methods)