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P. Lei, M. Abdelrahim, S. D. Cho, X. Liu and S. Safe, “Structure-Dependent Activation of Endoplasmic Reticulum Stress-Mediated Apoptosis in Pancreatic Cancer by 1,1-bis(3'-indoly)-1-(p-substituted phenyl)methanes,” Molecular Cancer Therapeutics, Vol. 7, No. 10, 2008, pp. 3363-3372. doi:10.1158/1535-7163.MCT-08-0439

has been cited by the following article:

• TITLE: The Apoptotic Effect of the Methanol Extract of Polygonum cuspidatum through Up-Regulation Death Receptor 5 and CHOP in HSC-2 Human Oral Cancer Cells

  AUTHORS: Hyun-Ju Yu, Ji-Ae Shin, Eun-Sun Choi, Jae-Gyu Jeon, Nam-Pyo Cho, Sung-Dae Cho

  KEYWORDS: Polygonum cuspidatum; Endoplasmic Reticulum Stress; C/EBP Homologous Protein/Growth Arrest and the DNA Damage-Inducible Gene 153 (CHOP); Death Receptor 5 (DR5); Apoptosis; Human Oral Cancer Cell

  JOURNAL NAME: Journal of Cancer Therapy, Vol.3 No.1, February 16, 2012

  ABSTRACT: Polygonum cuspidatum is used as a traditional medicinal herb for the therapy of various diseases including several types of cancers. In the present study, we focused on addressing the anti-cancer activity and molecular mechanism of methanol extract of Polygonum cuspidatum (MEPC) in HSC-2 human oral cancer cells. The effect of MEPC on oral cancer cells was estimated by 3-(4,5-dimethylthiazol-20yl)-(3-carboxymethoxyphenyl)-2-(4-sulphophenyl)-2H-tetrazolium (MTS) assay, 4’-6-diamidino-2-phenylindole (DAPI) staining and Western blot analysis. MEPC inhibited the cell viability and induced apoptosis through the induction of death receptor (DR) 5. MEPC also increased the expression of C/EBP homologous protein/growth arrest and the DNA damage-inducible gene 153 (CHOP), a transcription factor induced by ER stress. Thus, we concluded that the induction of CHOP leading to DR5 up-regulation is required for the anti-cancer activity of MEPC in HSC-2 cells and MEPC may be a promising drug candidate for oral cancer.