This study is suggestive that the PCR for detection of mecA gene is a fast, accurate and valuable diagnostic tool, particularly in hospitals in areas where methicillin-resistant S. aureus is endemic.

The aim of this review is to obtain a further understanding of the reported inhibitory effects of polyphenols on cancer cell proliferation and angiogenesis process and the probable mechanisms by which these natural compounds inhibit proliferation of cancer cells and angiogenesis. Growing evidence indicates that polyphenols are beneficial against human fatal diseases such as cancer. Because angiogenesis has a critical role in tumor growth and metastasis, therefore, we decided to review the potential anticancer and antiangiogenic activities and molecular mechanisms of different groups of known polyphenolic compounds. As knowledge and data on anticancer and antiangiogenic effects of plant-derived phenols are on the rise, it may be possible in the near future to develop and discover specific polyphenolic compounds with potent anticancer and antiangiogenic activity for treatment of malignant tumors.

Our previous studies had shown xanthomicrol and calycopterin, two plant-derived flavonoids, to have selective antiproliferative activity against some malignant cell lines. The present study is focused on the investigation of antiangiogenic potential of these two flavonoids, using in vitro and ex vivo models. Xanthomicrol and calycopterin were found to have potent inhibitory effects on microvessel outgrowth in the rat aortic ring assay. Xanthomicrol was able to completely block microvessel sprouting at 10 µg/mL, and calycopterin suppressed microvessel outgrowth by 89% at 5 µg/mL. Suramin and thalidomide, used at 20 µg/mL as positive controls, inhibited microvessel formation by 23% and 64%, respectively. The flavones also inhibited endothelial cell tube formation and human umbilical vein endothelial cell proliferation at 0.5, 5, and 10 µg/mL. In order to delineate the underlying mechanisms of antiangiogenic activity of these flavones, we investigated the influences of xanthomicrol and calycopterin on expression of vascular endothelial growth factor (VEGF) and basic-fibroblast growth factor (b-FGF) in endothelial cells. These flavones were able to inhibit VEGF expression at 0.5, 5, and 10 µg/mL, but they had little or no effect on b-FGF expression. These findings suggest that xanthomicrol and calycopterin possess potent antiangiogenic activities, which may be due to their inhibitory influences on VEGF expression.

Flavonoids constitute one of the most important classes of polyphenols, which have been found to have a wide range of biological activities such as anticancer effects. A large body of evidence demonstrates that morin as a pleiotropic dietary flavonoid possesses potent anticarcinogenic and anticancer activities with minimal toxicity against normal cells. The present review comprehensively elaborates the molecular mechanisms underlying antitumorigenic and anticancer effects of morin. Morin exerts its anticarcinogenic effects through multiple cancer preventive mechanisms, including reduction of oxidative stress, activation of phase II enzymes, induction of apoptosis, attenuation of inflammatory mediators, and downregulation of p‐Akt and NF‐κB expression. A variety of molecular targets and signaling pathways such as apoptosis, cell cycle, reactive oxygen species (ROS), matrix metalloproteinases (MMPs), epithelial‐mesenchymal transition (EMT), and microRNAs (miRNAs) as well as signal transducer and activator of transcription 3 (STAT3), NF‐κB, phosphatidylinositol 3‐kinase (PI3K)/Akt, mitogen‐activated protein kinase (MAPK), and Hippo pathways have been found to be involved in the anticancer effects of morin. In the adjuvant therapy, morin has been shown to have synergistic anticancer effects with several chemotherapeutic drugs. The findings of this review indicate that morin can act as a promising chemopreventive and chemotherapeutic agent.

No abstract

α-Conidendrin is a polyphenolic compound found mainly in Taxus yunnanensis, as the source of chemotherapy drug paclitaxel, which has been used in traditional medicine for treatment of cancer. This study aimed to investigate the anticancer activity and molecular mechanisms of α-conidendrin on breast cancer cell lines. The results of the present study show that α-conidendrin possesses potent antiproliferative effects on breast cancer cell lines MCF-7 and MDA-MB-231. α-Conidendrin significantly induced apoptosis in breast cancer cells via reactive oxygen species generation, upregulation of p53 and Bax, downregulation of Bcl-2, depolarization of mitochondrial membrane potential (MMP), release of cytochrome c from mitochondria, and activation of caspases-3 and -9. α-Conidendrin remarkably inhibited the proliferation of breast cancer cells through induction of cell cycle arrest by upregulating p53 and p21 and downregulating cyclin D1 and CDK4. Unlike breast cancer cells, the antiproliferative effect of α-conidendrin on human foreskin fibroblast cells (normal cells) was very small. In normal cells, reactive oxygen species levels, loss of MMP, release of cytochrome c, mRNA expression of p53, p21, cyclin D1, CDK4, Bax, and Bcl-2 as well as mRNA expression and activity of caspases-3 and -9 were significantly less affected by α-conidendrin compared with cancer cells. These results suggest that α-conidendrin can be a promising agent for treatment of breast cancer with little or no toxicity against normal cells. K E Y W O R D S apoptosis, breast cancer, cell cycle, polyphenolic compound, α-conidendrin

Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a promising anticancer cytokine with minimal toxicity towards normal cells. Nevertheless, most primary cancers are often intrinsically TRAIL-resistant or can acquire resistance after TRAIL therapy. This study aimed to investigate the inhibitory effect of co-treatment of 3-bromopyruvate (3-BP) as a potent anticancer agent with TRAIL on colon cancer cells (HT-29). The results of present study indicated that combined treatment with 3-BP and TRAIL inhibited the proliferation of HT-29 cells to a greater extent (88.4%) compared with 3-BP (54%) or TRAIL (11%) treatment alone. In contrast, the combination of 3-BP and TRAIL had no significant inhibitory effect on the proliferation of normal cells (HEK-293) (8.4%). At a cellular mechanistic level, the present study showed that 3-BP sensitized human colon cancer cells to TRAIL-induced apoptosis via reactive oxygen species generation, upregulation of Bax, downregulation of Bcl-2 and survivin, release of cytochrome c into the cytosol, and activation of caspase-3. In normal cells, 3-BP, TRAIL, or combination of both had no significant effect on the reactive oxygen species levels, release of cytochrome c, and caspase-3 activity. Therefore, the combination of 3-BP and TRAIL can be a promising therapeutic strategy for treatment of colon cancer.

No abstract