Abstract 4605: Consumption of S-allylcysteine inhibits the growth of human non-small cell lung carcinoma in a mouse xenograft model

Abstract

Abstract Lung cancer is one of the leading causes of cancer death in the world. Human non-small cell lung carcinoma (NSCLC) accounts for almost 80 percent of lung cancer cases. Aberrant phosphoinositide 3-kinase (PI3K)/ Akt /mTOR signaling pathways play important roles and have been widely observed in the development of NSCLC. Previous studies indicated that garlic extracts such as diallyl disulfide (DADS) and diallyl trisulfide (DATS) could inhibit the proliferation of several types of cancer in vitro. However, the inhibitory effects of S-allylcysteine (SAC) on the growth of NSCLC have not been demonstrated yet. Therefore, we investigated whether consumption of SAC could prevent the growth of NSCLC in both in vitro and in vivo models. In the current study, SAC significantly inhibited the proliferation of human NSCLC A549 cells in vitro. Treatment of NF-κB inhibitor, Bay-11-7082, could significantly inhibit the proliferation of NSCLC A549 cells. Our results demonstrated that SAC significantly suppressed the activation of mTOR, NF-κB and cyclin D1 molecules in vitro. Furthermore, our results demonstrated that consumption of SAC significantly inhibited the growth of highly metastatic human NSCLC cells in tumor bearing mice. Bioluminescence imaging, pathological and immunohistochemical (IHC) staining results also indicated that SAC could effectively suppress the growth and malignant progression of human NSCLC in vivo. The chemopreventive effects of SAC were associated with suppression of mTOR and NF-κB molecules in vivo. These results suggested that SAC could act as an effective agent against the malignant progression of human non small cell lung cancer in both in vitro and in vivo models. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4605. doi:10.1158/1538-7445.AM2011-4605