One mechanism by which Akt prevents apoptosis is considered to proceed through phosphorylation and inactivation of the pro apoptotic protein and also induc tion of the anti apoptotic Bcl 2 protein expression. The pro survival Bcl 2 family members are piv otal regulators of apoptotic cell death, therefore, they are considered as attractive targets for drug design. Interestingly, we found p AKT and Bcl 2 downregulation in HCT 116 and MSTO 211 upon CF treatment, thus leading us to believe that CF can be used for the preven tion of tumours and can possibly sensitize cancer cells to standard therapy. Conclusion Taken together, these findings establish an interaction between p53, c myc, Bcl 2, p21, p27 and PI3K Akt pathway and CF induced apoptosis in MSTO 211 and HCT 116 cells, which may improve prevention outcomes for meso thelioma and colon cancer.

Given the central role of p53, c myc, Akt and Bcl2 in cell proliferation and death of many cancers, together with the evidence obtained on MSTO 211 and HCT 116 cell lines treated with CF, we believe in the potential chemopreventive benefits of CF in human cancers. Although further investigation is underway BAY 57-1293 chemical structure in our laboratory, this present work suggests that CF can sensitize cancer cells to standard therapy. In addition, as a nutri tional supplement, CF can improve the quality of life of cancer patients undergoing antineoplastic therapy. Background RCC is one of the most common malignant tumors in urology. RCC accounts for 2 3% of all malignant tumors in adults, afflicts about 209,000 people, and causes 102,000 deaths per year worldwide.

The incidence and mortality rate of RCC have increased over the past sev eral years. RCC is classified into five major sub types, clear cell, papillary, chromophobe, collecting duct and unclassified RCC. Many renal masses remain PTC-209 HBr asymptom atic and nonpalpable until the late stages of the disease. Curative nephrectomy is the first treatment choice for RCC. However, metastatic disease recurs in a third of these patients. Still, About 30% of patients already have metastasis at the time of diagnosis. Although several promising biomarkers for RCC such as Carbonic anhy drase IX, B7 H1 and P53 have been investigated, none have been validated. RCC is resistant to chemo therapy, radiotherapy and immunotherapy. Although several targeted therapies, such as multitargeted tyro sine kinase inhibitors and Temsirolimus, which target the VHL HIF VEGF and or mTOR pathways, have been approved for the treatment of advanced RCC, complete responses are rare and resistance ultim ately will occur after a few months or a few years. Thus, the identification and application of novel thera peutic targets for RCC are urgently needed.