The contribution of keratinocytes in capecitabine-stimulated hand-foot-syndrome

Environ Toxicol Pharmacol. 2017 Jan:49:81-88. doi: 10.1016/j.etap.2016.12.001. Epub 2016 Dec 5.

Abstract

Capecitabine, as the first-line treatment for multiple tumor types, has a serious drawback of hand-foot-syndrome (HFS) that limits its clinical use. However, the pathophysiology and mechanism of capecitabine-induced HFS is rarely known. Here we built the experimental mouse model of HFS induced by capecitabine at first and it was shown that 3 of 6 mice appeared HFS in the 5th day and 5 mice occurred HFS in the 30th day. The corneous layer was reduced in capecitabine-induced HFS in vivo. Moreover, we found that capecitabine could significantly induce keratinocytes cells death in vitro through activated apoptosis pathway and decreased mitochondrial membrane potential. In conclusion, these results suggested that HFS of capecitabine may be developed from reduction of corneous layer through stimulation of intracellular mitochondrial dysfunction following activation of caspase-dependent apoptosis pathway.

Keywords: Capecitabine; Hand-foot-syndrome (HFS); Keratinocyte; Mitochondrial apoptosis.

MeSH terms

  • Animals
  • Antimetabolites, Antineoplastic / adverse effects*
  • Apoptosis / drug effects
  • Capecitabine / adverse effects*
  • Cell Line
  • Cell Proliferation / drug effects
  • Disease Models, Animal
  • Hand-Foot Syndrome / pathology*
  • Hand-Foot Syndrome / physiopathology
  • Humans
  • Keratinocytes / drug effects*
  • Keratinocytes / pathology
  • Keratinocytes / physiology
  • Male
  • Membrane Potential, Mitochondrial / drug effects
  • Mice, Inbred ICR

Substances

  • Antimetabolites, Antineoplastic
  • Capecitabine