Therefore, we believe that DIM may be a potential prophylactic and/or therapeutic agent for bone diseases, such as postmenopausal osteoporosis. The authors indicated no potential conflicts of interest. We would like to thank Dr. Y. Imai for his technical support and advice. This work was supported by a postdoctoral fellowship for foreign researchers (Grant number 12F02106 to TY) from the Japan Society for the Promotion of Science (JSPS). “
“Colorectal cancer (CRC) is one of the most common cancers and a leading cause of cancer death in both men and women. Although promising progress

has been made in the diagnosis and treatment of CRC over the last decade, this TSA HDAC cost cancer remains a major public health problem (1), (2) and (3). There is an urgent demand to better understand the molecular mechanisms underlying the different phenotypes of CRC. This understanding may provide information supporting drug discovery and prevention strategies (1). The development of human genome technologies, such as DNA microarrays, has allowed us to simultaneously examine thousands of genes, leading to a better understanding of carcinogenesis (4). Studies related to compound treatment outcomes by differences in gene expression profiling facilitate the search for more curative interventions LY294002 clinical trial (5). Increasing evidence shows that patients with cancer often resort to complementary

and alternative medical supplements to treat cancer, cancer-related symptoms, or to reduce the adverse effects of chemotherapy (6). Botanicals can contain effective anticancer compounds Carnitine dehydrogenase that can be used alone or as

adjuncts to existing chemotherapy, thereby improving efficacy and reducing drug-induced adverse events (7) and (8). In current cancer treatment, approximately 80% of novel drugs have originated from natural products (9). American ginseng (Panax quinquefolius L.) is a commonly used herbal medicine in the United States. Protopanaxadiol (PPD, Fig. 1), an aglycon of ginseng saponins from the ginseng, has shown anticancer potential in our previous studies (10). However, the previous study emphasized in vitro bioactivity screening using PPD and its derivatives, the in vivo antitumor effects were not evaluated. In addition, PPD’s anti-CRC mechanisms have largely not been explored. To better understand the anticancer effects of PPD, in the present study, we first used an athymic nude mouse xenograft tumor model to observe the compound’s in vivo activity. Next, a panel of human colorectal cancer cell lines (i.e., SW-480, HT-29, and HCT-116), which differ in the expression of the tumor suppressor gene, p53, were used to compare the anti-proliferation activities. Then, HCT-116 cells, which showed the most significant growth inhibition by PPD, were selected to explore the compound’s effect on mRNA.