Protective Role of Fucoidan on Cisplatin-mediated ER Stress in Renal Proximal Tubule Epithelial Cells

Anticancer Res. 2019 Oct;39(10):5515-5524. doi: 10.21873/anticanres.13744.

Abstract

Background/aim: Administration of cisplatin in cancer patients is limited by the kidney-related adverse effects; however, a protective strategy is absent. We hypothesized that fucoidan protects the proximal tubule epithelial (TH-1) cells against the effects of cisplatin.

Materials and methods: To assess the effect of fucoidan, its effect on reactive oxygen species (ROS) formation, endoplasmic reticulum (ER) stress response, DNA damage response (DDR), apoptosis, and cell-cycle arrest in TH-1 cells was investigated.

Results: Cisplatin increased the accumulation of ROS, leading to excessive ER stress. In presence of cisplatin, treatment of TH-1 cells with fucoidan significantly reduced the ER stress by maintaining the complex of GRP78 with PERK and IRE1α. In particular, fucoidan enhanced the antioxidative capacity through up-regulation of PrPC Furthermore, fucoidan suppressed cisplatin-induced apoptosis and cell-cycle arrest, whereas silencing of PRNP blocked these effects of fucoidan.

Conclusion: Fucoidan may be a potential adjuvant therapy for cancer patients treated with cisplatin as it preserves renal functionality.

Keywords: DNA damage; ER stress; Fucoidan; ROS; cellular prion protein; cisplatin.

MeSH terms

  • Antioxidants / metabolism
  • Apoptosis / drug effects
  • Cell Cycle Checkpoints / drug effects
  • Cell Line
  • Cisplatin / pharmacology*
  • Endoplasmic Reticulum Chaperone BiP
  • Endoplasmic Reticulum Stress / drug effects*
  • Epithelial Cells / drug effects*
  • Epithelial Cells / metabolism
  • Heat-Shock Proteins / metabolism
  • Humans
  • Kidney / drug effects
  • Kidney / metabolism
  • Kidney Tubules, Proximal / drug effects*
  • Kidney Tubules, Proximal / metabolism
  • Polysaccharides / pharmacology*
  • Protective Agents / pharmacology*
  • Protein Serine-Threonine Kinases / metabolism
  • Reactive Oxygen Species / metabolism
  • Th1 Cells / drug effects
  • Th1 Cells / metabolism
  • Up-Regulation / drug effects
  • eIF-2 Kinase / metabolism

Substances

  • Antioxidants
  • Endoplasmic Reticulum Chaperone BiP
  • HSPA5 protein, human
  • Heat-Shock Proteins
  • Polysaccharides
  • Protective Agents
  • Reactive Oxygen Species
  • fucoidan
  • Protein Serine-Threonine Kinases
  • eIF-2 Kinase
  • Cisplatin