Cell Research

Secretion clusterin (sClu) is a kind of disease of protein, played an important role in protecting cells from tumor necrosis factor (TNF) α induced apoptosis. The purpose of this study was to survey the molecular mechanism of the influence sClu TNF induced apoptosis in breast cancer cells. The wild type of p53 expression MCF 7 cell line was designed out excessive performance sClu (MCF 7 / sClu), and mda - m - 231 cell line and mutant p53 and sClu son transfection is the silence of the small interference RNA (mda - m - 231 / sClu small interference RNA). Clusterin overexpression influence, in the cell apoptosis and sensitivity are two TNF α in vitro. Our results show that TNF treatment increase BCL 2 mRNA and protein content in breast cancer cells, which suggests that BCL 2 directly subject to nuclear factor - kappaB (NF - kappaB) in response to TNF α. The induction of the base class library 2 mediated p65 subelement of NF - kappaB. The silence of the small interference RNA mediated BCL 2 lead to increased significantly TNF induced apoptosis. The silence of the sClu in mda - m - 231 / sClu small interference RNA cell abolished TNF mediated NF - kappaB activation and BCL 2 overexpression, and present mda - m - 231 / sClu small interference RNA cell significantly more sensitive, TNF than parent mediated apoptosis. In addition, sClu expression in the MCF 7 / sClu cell mediated TNF NF - kappaB promotion activities and BCL 2 overexpression, and presents MCF 7 / Clu cell significant resistance to TNF α mediated apoptosis. Inhibition of NF - kappaB activity or p65 and BCL 2 expression reverse these effects. The results show that sClu awarded breast cancer cells apoptosis induced resistance of TNF α by NF - kappaB activation and BCL 2 overexpression.

The skin is often damaged by genetic and environmental factors such as smoking, contact xenobiotics, heat, hormonal changes, and ultraviolet ray. These factors will cause skin disease. White rattan is quadrangularis falls. (CQ) had been used in folk medicine to treat skin disease since ancient times. In considering take medicinal values show this genus, this is decided to investigate the antitumor activity of CQ. Extraction get and their phenolic content by in vitro CQ antitumor activity evaluation by using A431 (skin epidermoid carcinoma, humans) cell line. A431 cells are used different extract of CQ in dose dependent way. Five extract, acetone extract demonstrates important anticancer activity in A431 cell line. N-hexane, chloroform, ethyl acetate and methanol extract also showed a cell toxicity, but for a relatively small extent than acetone extract. GI (50) value of the acetone extract was found to 8 μ g ml (1), and GI (50) value of the purification part of acetone extract, known as the AFCQ (active part acetone CQ) A431 cells, were found to be 4.8 u g ml (1). In addition, the mechanism of antitumor activity, AFCQ exhibited by comparing its effect and the standard anti-cancer drugs adriamycin (doxorubicin) through the evaluation of the state mark apoptosis after treatment A431 cells and AFCQ and adriamycin. Burlington BCL 2 ratio along with the release of cytochrome c from the mitochondrial cytoplasm, this is a hallmark of cell apoptosis, also be evaluated. Cleavage of PARP revealed that AFCQ A431 cells apoptosis occurred, reference doxorubicin.

Antisense oligonucleotides (management) has been used for prostate cancer model for growth regulatory proteins, and at least one oligosaccharides (against BCL 2) has reached the clinical test. We've found that in LNCaP cell, mono - and double function management, the relative inhibitory expression, as compensation, the base class library 2 inhibition caspase 3 (apoptosis promoter) activities, and increase the expression of androgen receptor (AR) and p300 and il - co catalyst. In addition, the prostate specific membrane antigen (PSMA) and (may be its regulators) interferon (IFN) rise. 14 protein distributed between regulators of apoptosis, androgen control, differentiation antigen and autocrine mediated growth has been inspection. We put these findings including vascular endothelial growth factor (VEGF), promote angiogenesis, not through the compensation significant change, so do not need additional supervision for repression BCL 2 treatment is effective (such as caspase 3).