Anti-CDC25C (aa 214-218) polyclonal antibody

Fisetin, a naturally occurring flavonoid, is found in common fruits and vegetables and has been shown to induce cytotoxic effects in many human cancer cell lines. No information has shown that fisetin induced cell cycle arrest and apoptosis in mouse leukemia WEHI-3 cells. We found that fisetin decreased total viable cells through G(0)/G(1) phase arrest and induced sub-G(1) phase (apoptosis). We have confirmed fisetin induced cell apoptosis by the formation of DNA fragmentation and induction of apoptotic cell death. Results indicated that fisetin induced intracellular Ca2+ increase but decreased the ROS production and the levels of Delta Psi m in WEHI-3 cells. Fisetin increased the activities of caspase-3, -8 and -9. Cells were pre-treated with inhibitors of caspase-3, -8 and -9 and then treated with fisetin and results showed increased viable cell number when compared to fisetin treated only. Fisetin reduced expressions of cdc25a but increased p-p53, Chk1, p21 and p27 that may lead to G(0)/G(1) phase arrest. Fisetin inhibited anti-apoptotic protein Bcl-2 and Bcl-xL and increased pro-apoptotic protein Bax and Bak. Furthermore, fisetin increased the protein expression of cytochrome c and AIF. Fisetin decreased cell number through G(0)/G(1) phase arrest via the inhibition of cdc25c and induction of apoptosis through caspase-dependent and mitochondria-dependent pathways. Therefore, fisetin may be useful as a potential therapeutic agent for leukemia.

Colorectal cancer represents a great burden for patients worldwide. Long noncoding RNA BX357664 is an RNA that was identified by microarray technique in renal cell carcinoma. The function of BX357664 in solid tumors remains largely unknown. The present study aimed to investigate the expression profile and functional role of BX357664 in human colorectal cancer progression. The transcription levels of BX357664 were initially examined in vivo and in vitro. An overexpression plasmid was constructed in order to examine the effects of BX357664 overexpression on cell proliferation, apoptosis, migration and invasion. The results demonstrated that BX357664 was significantly downregulated in clinical colorectal cancer tissues and cell lines. Overexpression of BX357664 decreased cell proliferation rates and cell colony formation capacities in HCT116 and HT-29 cells. Following BX357664 overexpression, HCT116 and HT-29 cells exhibited reduced migration and invasion capacities. Would closure was also blunted by > 50% following overexpression of BX357664 in HCT-116 and HT-29 cells. In addition, the cell cycle regulators Cyclin B1, CDC25C and Cyclin D1 as well as the mesenchymal marker N-cadherin were downregulated, whereas the epithelial marker E-cadherin was upregulated by BX357664 overexpression. Finally, HCT116 and HT-29 cell apoptosis was induced and activities of caspase-3 and caspase-9 increased significantly following BX357664 overexpression. The present data suggested that BX257664 negatively regulated cell proliferation and metastasis and promoted cell apoptosis in colorectal cancer. These observations provided novel evidence that BX357664 might serve as a tumor suppressor and a potential therapeutic target in the treatment of colorectal cancer in the clinic.