Analysis of apoptosis-associated molecules Erythroid differentiation regulator 1, bcl-2 and p53 in actinic keratosis after treatment with ingenol mebutate

Yu Ri Woo, Ji Hong Lim, Seo Won Jeong, Dae Ho Cho, Hyun Jeong Park

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Actinic keratosis (AK) is the most common cutaneous premalignant neoplasm precursor of malignant skin tumors. The aberrant apoptotic pathway is thought to be associated with pathogenesis of AK. Ingenol mebutate has been shown to be effective and safe for treatment of AK. However, the effect of ingenol mebutate on apoptosis-related molecules using human skin samples has not been studied well. Erythroid differentiation regulator 1 (Erdr1) was recently reported to play a crucial role in malignant skin cancers like malignant melanoma. The role of Erdr1 in premalignant actinic keratosis (AK) has not been explored. The purpose of this study was to investigate whether the expression of apoptosis-associated molecules such as Erdr1, p53 and bcl-2 was affected by the treatment of ingenol mebutate in AK. Nine patients with AK underwent skin biopsy at baseline and 8 weeks after treatment with ingenol mebutate for immunohistochemical evaluation with Erdr1, p53 and bcl-2. In addition, skin samples from five control subjects were retrieved. Upregulation of Erdr1 and a significant decrease in expression of p53 and bcl-2 were observed after treatment with ingenol mebutate. Ingenol mebutate treatment for AK resulted in the modulation of apoptosis-associated molecules with an increase in the expression of Erdr1 and a decrease in the expression of p53 and bcl-2.

Original languageEnglish
Pages (from-to)1012-1017
Number of pages6
JournalExperimental Dermatology
Volume26
Issue number11
DOIs
Publication statusPublished - 2017 Nov 1
Externally publishedYes

Keywords

  • actinic keratosis
  • apoptosis
  • bcl-2
  • erythroid differentiation regulator 1
  • ingenol mebutate
  • p53

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Dermatology

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