Pculin02H, a curcumin derivative, inhibits proliferation and clinical drug resistance of HER2-overexpressing cancer cells

Jin Cherng Lien, Chao Ming Hung, Yi Jing Lin, Hui Chang Lin, Ting Chia Ko, Li Chung Tseng, Sheng Chu Kuo, Chi Tang Ho, Jang Chang Lee, Tzong Der Way

Research output: Contribution to journalArticlepeer-review

9 Scopus citations

Abstract

Amplification of the HER2 gene (also known as neu or ErbB2) or overexpression of HER2 protein has become a solicitous therapeutic target in metastatic and clinical drug-resistance cancer. In our present work, a new series of curcumin derivatives were designed and synthesized using curcumin as model. Here, we evaluated whether curcumin derivatives have better efficiency to degrade HER2 than curcumin. Among these test compounds, pculin02H had better efficiency to inhibit the expression of HER2 than curcumin. Moreover, pculin02H preferentially suppressed the growth of HER2-overexpressing cancer cell lines. Pculin02H induced G2/M cell cycle arrest followed by apoptosis. Interestingly, our results suggested that a posttranslational mechanism contributed to pculin02H-induced HER2 depletion in HER2-overexpressing cancer cells. We found that pculin02H significantly enhanced the antitumor efficacy of clinical drugs on HER2-overexpressing cancer cells as well as efficiently reduced HER2-induced drug resistance. These findings may provide an alternative preventive or therapeutic strategy against HER2-overexpressing cancer cells.

Original languageEnglish (US)
Pages (from-to)17-26
Number of pages10
JournalChemico-Biological Interactions
Volume235
DOIs
StatePublished - Jun 25 2015

All Science Journal Classification (ASJC) codes

  • Toxicology

Keywords

  • Apoptosis
  • G2/M arrest
  • HER2
  • Pculin02H

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