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Menahydroquinone-4 may play a key role in regulating CCL5 expression induced by epidermal growth factor receptor

Shotaro Goto1, Shuichi Setoguchi2, Daisuke Watase2

  • 1Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1 Nanakuma, Jonan-Ku, Fukuoka, 814-0180, Japan. sgoto@fukuoka-u.ac.jp.

Scientific Reports
|December 13, 2023
PubMed

Insights

Vitamin K2 (menaquinone-4) and its active form, menahydroquinone-4 (MKH), may alleviate skin rash side effects from EGFR inhibitors. This study reveals MKH suppresses CCL5, a key factor in drug-induced skin damage.

Area of Science:

  • Biochemistry
  • Dermatology
  • Molecular Biology

Background:

  • Epidermal growth factor receptor (EGFR) inhibitors cause severe skin rash, impacting patient treatment.
  • Vitamin K has shown promise in mitigating these side effects, but mechanisms are unclear.
  • EGFR inhibitors induce C-C motif chemokine ligand 5 (CCL5) in skin

Purpose of the Study:

  • To investigate the mechanism of menahydroquinone-4 (MKH), the active form of vitamin K2 (menaquinone-4), in alleviating EGFR inhibitor-induced skin rash.
  • To explore the role of MKH in regulating CCL5 expression.

Main Methods:

  • Utilized human skin cell lines (HaCaT and HSC-1).
  • Evaluated the effects of EGFR inhibitors and MKH derivatives (including MK-4) on cellular responses.
  • Assessed the impact of UBIAD1 (MKH synthetase) and γ-glutamyl carboxylase expression and warfarin treatment on CCL5 levels.

Main Results:

  • EGFR inhibitors downregulated UBIAD1 expression and MKH biosynthesis.
  • Knockdown of UBIAD1 or γ-glutamyl carboxylase, and warfarin treatment, increased CCL5 expression.
  • MKH derivatives effectively suppressed EGFR inhibitor-induced CCL5 expression.

Conclusions:

  • Menahydroquinone-4 (MKH) plays a crucial role in suppressing CCL5.
  • MKH is involved in alleviating skin damage caused by EGFR inhibitors.
  • This suggests a therapeutic potential for MKH in managing EGFR inhibitor-related dermatological side effects.

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