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Targeting cancer-related inflammation: Chinese herbal medicine inhibits epithelial-to-mesenchymal transition in pancreatic cancer.

Abstract
Pancreatic cancer is an almost universally fatal disease resulting from early invasion of adjacent structures and metastasis and the lack of an effective treatment modality. Our previous studies have shown that Qingyihuaji Formula (QYHJ), a seven-herb Chinese medicine formula, had significant anti-cancer effects in pancreatic cancer. Here, we examined the effects of QYHJ on pancreatic cancer cell invasion and metastasis and the potential associated mechanism(s). We found that QYHJ inhibited both tumor growth and metastasis in nude mice with human pancreatic cancer cell xenografts. Further study indicated that QYHJ inhibited epithelial-to-mesenchymal transition (EMT), which is characterized by increased E-cadherin expression and decreased vimentin, N-cadherin and Slug expression. Interleukin 6 (IL-6), a pro-inflammatory cytokine produced mainly by macrophages, could promote cancer cell EMT and invasion. In contrast, treatment with QYHJ inhibited cancer-related inflammation in tumors by decreasing infiltration of tumor-associated macrophages and IL-6 production, thus preventing cell invasion and metastasis. These results suggested that the Chinese herbal medicine QYHJ could inhibit pancreatic cancer cell invasion and metastasis in part by reversing tumor-supporting inflammation.
AuthorsJuan Zhang, Peng Wang, Huaqiang Ouyang, Jianhua Yin, Aihua Liu, Chunzheng Ma, Luming Liu
JournalPloS one (PLoS One) Vol. 8 Issue 7 Pg. e70334 ( 2013) ISSN: 1932-6203 [Electronic] United States
PMID23922983 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Drugs, Chinese Herbal
  • Interleukin-6
  • Qingyihuaji
Topics
  • Animals
  • Cell Line, Tumor
  • Cell Movement (drug effects)
  • Disease Models, Animal
  • Drugs, Chinese Herbal (administration & dosage, pharmacology)
  • Epithelial-Mesenchymal Transition (drug effects)
  • Female
  • Herbal Medicine
  • Humans
  • Inflammation (drug therapy, pathology)
  • Interleukin-6 (pharmacology)
  • Liver Neoplasms (drug therapy, pathology, secondary)
  • Mice
  • Models, Biological
  • Pancreatic Neoplasms (drug therapy, pathology)
  • Tumor Burden (drug effects)

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