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Research Paper|Volume 12, Issue 17|pp 17625—17633

Graphene oxide inhibits cell migration and invasion by destroying actin cytoskeleton in cervical cancer cells

Jing Wang1,5, Ping Wang2, Ying He1, Xiaoli Liu3, Sisi Wang1, Chunxing Ma1, Xiaofei Tian4, Jing Wang5, Xin Wu6
  • 1Department of Gynaecology and Obstetrics, The First Affiliated Hospital of Hebei North University, Zhangjiakou, Hebei Province, China
  • 2Operating Room, The First Affiliated Hospital of Hebei North University, Zhangjiakou, Hebei Province, China
  • 3Department of Gynecology and Obstetrics, Hebei Maternity Hospital, Shijiazhuang, Hebei Province, China
  • 4Basic Medical College, Hebei North University, Zhangjiakou, Hebei Province, China
  • 5Life Science Research Center, Hebei North University, Zhangjiakou, Hebei Province, China
  • 6Department of Pathology, Hebei North University, Zhangjiakou, Hebei Province, China
Received: February 13, 2020Accepted: July 14, 2020Published: September 14, 2020
https://doi.org/10.18632/aging.103821

Copyright: © 2020 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Objective: To investigate the antitumor effects of Graphene oxide (GO) on tumor invasion and metastasis in human cervical cancer Hela cells.

Results: GO significantly inhibited cell viability and the number of clones, promoted cell apoptosis, as well as suppressed cell migration and invasion, and destroyed the structure of actin cytoskeleton of Hela cells in a dose-dependent manner in. Moreover, the expression of metastasis-related proteins, including MMP2 and Cdc42, were significantly suppressed by the treatment of GO. And the expression of MMP3 was remarkably increased by Smad inhibitor and the protein levels of MMP3 and ICAM were elevated by the JNK inhibitor in GO-treated Hela cells.

Conclusion: GO exhibited inhibitory effects on cell migration and invasion possibly by destroying actin cytoskeleton in Hela cells, which is a potential component of the Smad and JNK signalling pathways.

Methods: GO was prepared and chracterized by UV visible light absorption spectroscopy and atomic force microscopy. Hela cells were treated with Go at different dose levels. Then, in vitro cytotoxicity of GO was evaluated by the MTT assay, colony-forming assay and cell apoptosis assay. The inhibitory effects of GO on tumor cell migration and invasion as well as actin cytoskeleton were explored using Hela cells.