GRP78 mediates the therapeutic efficacy of curcumin on colon cancer

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• 作者：Yu-Jia Chang (1) (2) (3) (4)
  Chien-Yu Huang (5) (6)
  Chin-Sheng Hung (2) (3) (4)
  Wei-Yu Chen (7) (8)
  Po-Li Wei (2) (3) (4)
  
  1. Graduate Institute of Clinical Medicine ; College of Medicine ; Taipei Medical University ; Taipei ; Taiwan
  2. Department of Surgery ; School of Medicine ; College of Medicine ; Taipei Medical University ; Taipei ; Taiwan
  3. Division of General Surgery ; Department of Surgery ; Taipei Medical University Hospital ; Taipei Medical University ; Taipei ; Taiwan
  4. Cancer Research Center ; Taipei Medical University Hospital ; Taipei Medical University ; 250 Wu-Xing Street ; Taipei ; 110 ; Taiwan
  5. Division of General Surgery ; Department of Surgery ; Shuang Ho Hospital ; Taipei Medical University ; Taipei ; Taiwan
  6. Department of Neurosurgery ; Shuang Ho Hospital ; Taipei Medical University ; Taipei ; Taiwan
  7. Department of Pathology ; School of Medicine ; College of Medicine ; Taipei Medical University ; Taipei ; Taiwan
  8. Department of Pathology ; Wan Fang Hospital ; Taipei Medical University ; Taipei ; Taiwan
  
• 关键词：Colon cancer ; Antiproliferation ; Curcumin ; GRP78
• 刊名：Tumor Biology
• 出版年：2015
• 出版时间：February 2015
• 年：2015
• 卷：36
• 期：2
• 页码：633-641
• 全文大小：906 KB
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• 刊物主题：Cancer Research;
• 出版者：Springer Netherlands
• ISSN：1423-0380

文摘

Glucose-regulated protein 78 (GRP78) is the key regulator of endoplasmic reticular (ER) function. Expression of GRP78 was correlated with malignancy in different cancers. However, the role of GRP78 in the cytotoxic effect of curcumin on colon cancer cells is still unclear. A silencing RNA (siRNA) technique was used to knock down GRP78 expression. The anticancer effects of curcumin were assessed by a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, a flow cytometric cell cycle analysis, and a terminal dexynucleotidyl transferase-mediated nick end labeling (TUNEL) assay. HT-29 cells expressed lower GRP78 compared with DLD-1 cells. The MTT assay revealed that HT-29 cells were more resistant to curcumin treatment than DLD-1 cells. GRP78KD cells showed more resistance to curcumin treatment compared with scrambled control cells. Overexpressed GRP78 in HT-29 cells increased the sensitivity to curcumin treatment. According to the cell cycle analysis and TUNEL assay, we found that apoptosis dramatically increased in scrambled control cells compared to GRP78KD DLD-1 cells after curcumin treatment. Finally, we evaluated levels of Bcl-2, BAX, and Bad and found that an increase of Bcl-2 level was observed in GRP78KD cells treated with curcumin. Those results were consistent with the increasing of resistance to curcumin after silencing of GRP78. The levels of GRP78 expression might determine the therapeutic efficacy of curcumin against colon cancer cells.