Abstract
Bamboo shavings (Bambusae Caulis in Taeniam, BCT) are widely used as a traditional Chinese medicine to control hypertension and cardiovascular disease, and to alleviate fever, vomiting, and diarrhea. It has been demonstrated that BCT reduces ovalbumin-induced airway inflammation by regulating pro-inflammatory cytokines, and decreases tumor growth in tumor-bearing mice. However, the effects of BCT on the metastatic potential of malignant cancer cells and the detailed mechanism of its anti-metastatic activity have not been examined previously. In this study, we investigated whether an aqueous extract of BCT (AE-BCT) reduces the metastatic potential of HT1080 cells, and elucidated the underlying anti-metastatic mechanism. In addition, we examined whether AE-BCT administration inhibits pulmonary metastasis of intravenously injected B16F10 cells in C57BL/6J mice. AE-BCT (50–250 µg/ml) dose-dependently suppressed colony-forming activity under anchorage-dependent and -independent growth conditions. Pretreatment with AE-BCT efficiently inhibited cell migration, invasion, and adhesion. AE-BCT also dramatically suppressed PMA-induced MMP-9 activity and expression by blocking NF-κB activation and ERK phosphorylation. Production of intracellular ROS, a key regulator of NF-κB-induced MMP-9 activity, was almost completely blocked by pretreatment with AE-BCT. Furthermore, daily oral administration of AE-BCT at doses of 50 and 100 mg/kg efficiently inhibited lung metastasis of B16F10 cells injected into the tail veins of C57BL/6J mice with no systemic toxicity. These results demonstrate that AE-BCT significantly reduced the metastatic activity of highly malignant cancer cells by suppressing MMP-9 activity via inhibition of ROS-mediated NF-κB activation. These results indicate that AE-BCT may be a safe natural product for treatment of metastatic cancer.
Highlights
Cancer metastasis, the spread of cancer cells from the primary neoplasm to distant organs via blood or lymph vessels and their subsequent outgrowth, is a major cause of death in cancer patients and remains a challenge in cancer treatment [1,2]
Several studies reported that reactive oxygen species (ROS) participate in the activation of NF-kB, a key player in tumorigenesis, and that excess ROS produced by cancer cells trigger tumor invasion and angiogenesis via NF-kB-mediated matrix metalloproteinases (MMPs)-9 activation [10,11]
Since cell-to-extracellular matrix (ECM) adhesion is believed to be a fundamental step in tumor invasion [21], we examined the effect of aqueous extract of BCT (AE-BCT) on the adhesion of HT1080 cells to fibronectin (FN) and type I collagen
Summary
The spread of cancer cells from the primary neoplasm to distant organs via blood or lymph vessels and their subsequent outgrowth, is a major cause of death in cancer patients and remains a challenge in cancer treatment [1,2]. Degradation of the ECM and components of basement membranes plays an essential role in metastasis and is caused by the action of proteinases, such as matrix metalloproteinases (MMPs), serine proteinases, cathepsins, and plasminogen activators (PAs) [4,5,6]. Among these proteinases, MMP-9 is abundantly expressed in various malignant tumors and is considered to be closely associated with tumor progression, metastasis, and angiogenesis [7,8,9]. ROS scavenging and/or inhibition of NF-kB activation lead to the suppression of MMP-9 activity and further tumor invasion [12]
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