Alkylphenols from the Roots of Ardisia brevicaulis Induce G1 Arrest and Apoptosis through Endoplasmic Reticulum Stress Pathway in Human Non-small-cell Lung Cancer Cells

DOI Web Site Web Site PubMed 参考文献19件
  • Zhu Guo-Yuan
    School of Chinese Medicine, Hong Kong Baptist University
  • Wong Blenda Chi Kwan
    School of Chinese Medicine, Hong Kong Baptist University
  • Lu Aiping
    School of Chinese Medicine, Hong Kong Baptist University
  • Bian Zhao-Xiang
    School of Chinese Medicine, Hong Kong Baptist University
  • Zhang Ge
    Musculoskeletal Research Laboratory, Department of Orthopaedics and Traumatology, The Chinese University of Hong Kong
  • Chen Hu-Biao
    School of Chinese Medicine, Hong Kong Baptist University
  • Wong Yuen Fan
    School of Chinese Medicine, Hong Kong Baptist University
  • Fong Wang-Fun
    School of Chinese Medicine, Hong Kong Baptist University
  • Yang Zhijun
    School of Chinese Medicine, Hong Kong Baptist University

書誌事項

タイトル別名
  • Alkylphenols from the Roots of <i>Ardisia brevicaulis</i> Induce G1 Arrest and Apoptosis through Endoplasmic Reticulum Stress Pathway in Human Non-small-cell Lung Cancer Cells

この論文をさがす

説明

From the roots of Ardisia brevicaulis DIELS, two new alkylphenol derivatives, named ardisiphenol E (2) and F (3), have been isolated together with a known alkylphenol, ardisiphenol D (1). The structures of 1–3 were elucidated by chemical and spectroscopic techniques. Compounds 1 and 2 exhibited strong cytotoxicities on two human non-small-cell lung cancer cell lines (H1299 and A549). We found that compounds 1 and 2 upregulated mRNA and protein expressions of endoplasmic reticulum (ER) stress markers including C/EBP homologous protein (CHOP), binding immunoglobulin protein (Bip) and inositol-requiring enzyme 1 (IRE1) indicating 1 and 2 are novel natural ER stress inducers. Treatments with 1 and 5 µM of 1 or 2 triggered G1 arrest in H1299 and A549 cells with concomitant downregulation of ubiquitin fusion degradation protein 1 (Ufd1) and S-phase kinase-associated protein 2 (Skp2) proteins and the accumulation of p27, the key axes of ER stress-mediated G1 arrest. Compounds 1 and 2 also induced apoptosis at high concentrations (10, 20 µM) which was shown to be coupled with the upregulation of CHOP and Bim, the activation of caspase-9, caspase-3 and poly(ADP-ribose) polymerase (PARP) cleavage. These results indicate that compounds 1 and 2 induce ER stress that subsequently causes G1 arrest and apoptosis in human non-small-cell lung cancer cells and they may have potential anticancer effects.

収録刊行物

参考文献 (19)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ