Antitumor activity of emodin against pancreatic cancer depends on its dual role: promotion of apoptosis and suppression of angiogenesis

Autor: Hui Chen, Wei-Tian Wei, Hai-Bin Liu, Hong-Chun Guo, Zhong-Lin Ni, Dian-Lei Liu, Hongfei Tong, Shengzhang Lin, Zhao-Hong Wang, Kangjie Chen
Rok vydání: 2012
Předmět:
Phytochemistry
Anatomy and Physiology
Angiogenesis
Phytopharmacology
Phytochemicals
Cancer Treatment
lcsh:Medicine
Angiogenesis Inhibitors
Apoptosis
Pharmacology
Neovascularization
chemistry.chemical_compound
Mice
Enos
Immune Physiology
Molecular Cell Biology
Drug Discovery
Basic Cancer Research
lcsh:Science
Mice
Inbred BALB C

Multidisciplinary
biology
Neovascularization
Pathologic

Cell Death
Chemistry
Vascular Endothelial Growth Factors
NF-kappa B
Tumor Burden
Gene Expression Regulation
Neoplastic

Matrix Metalloproteinase 9
Oncology
Matrix Metalloproteinase 2
Cytokines
Medicine
Female
Antiangiogenesis Therapy
medicine.symptom
medicine.drug
Research Article
Drugs and Devices
Emodin
Drug Research and Development
Nitric Oxide Synthase Type III
Immunology
Mice
Nude

Antineoplastic Agents
Gastroenterology and Hepatology
Complementary and Alternative Medicine
In vivo
Pancreatic cancer
Cell Line
Tumor

medicine
Animals
Humans
Biology
Pancreas
lcsh:R
Chemotherapy and Drug Treatment
biology.organism_classification
medicine.disease
Xenograft Model Antitumor Assays
Gemcitabine
Enzyme Activation
Pancreatic Neoplasms
Immune System
lcsh:Q
Clinical Immunology
Zdroj: PLoS ONE
PLoS ONE, Vol 7, Iss 8, p e42146 (2012)
ISSN: 1932-6203
Popis: Background Emodin has been showed to induce apoptosis of pancreatic cancer cells and inhibit tumor growth in our previous studies. This study was designed to investigate whether emodin could inhibit the angiogenesis of pancreatic cancer tissues and its mechanism. Methodology/Principal Finding In accordance with our previous study, emodin inhibited pancreatic cancer cell growth, induced apoptosis, and enhanced the anti-tumor effect of gemcitabine on pancreatic caner cells in vitro and in vivo by inhibiting the activity of NF-κB. Here, for the first time, we demonstrated that emodin inhibited tumor angiogenesis in vitro and in implanted pancreatic cancer tissues, decreased the expression of angiogenesis-associated factors (NF-κB and its regulated factors VEGF, MMP-2, MMP-9, and eNOS), and reduced eNOS phosphorylation, as evidenced by both immunohistochemistry and western blot analysis of implanted tumors. In addition, we found that emodin had no effect on VEGFR expression in vivo. Conclusions/Significance Our results suggested that emodin has potential anti-tumor effect on pancreatic cancer via its dual role in the promotion of apoptosis and suppression of angiogenesis, probably through regulating the expression of NF-κB and NF-κB-regulated angiogenesis-associated factors.
Databáze: OpenAIRE