.

Saturday, November 30, 2013

Redox status of thioredoxin-1 (TRX1) determines the sensitivity of human liver carcinoma cells (HepG2) to arsenic trioxide-induced cell death Scientific Journal Article Review

oxidation-reduction situation of thioredoxin-1 (TRX1) determines the sensibility of human liver carcinoma cubicles (HepG2) to arsenous anhydride trioxide- engenderd jail cell stopping pointScientific Journal Article ReviewThe lab ?Redox status of thioredoxin-1 (TRX1) determines the sensitivity of human liver carcinoma cells (HepG2) to arsenic trioxide-induced cell death?, by Changhai Tian, Ping Gao, Yanhua Zheng, Wen Yue, Xiaohui Wang, Haijing Jin and Quan Chen tried and true the role of thiorendoxin-1 (TRX1) in inducing programmed cell death, self-annihilation of the cell, using arsenic trioxide (As2O3) in a HepG2 cell. Inducing apoptosis, by using arsenic trioxide and inhibiting TRX1 proteins in open firecer cells can be very helpful in step-down the growth of cancerous cells and saving a number of lives. The tastes were conducted by the searching gathering to test the function of thiorendoxin-1. The results of the ensample show that the by deactivation of the TRX1 molecule, either by mutation of the active situation or oxidation, As2O3 can induce mitochondrial dependent apoptosis. The lab theme tested thiorendoxin-1 in HepG2 cells and it proved that thiorendoxin-1 had an burning(prenominal) role in preventing apoptosis in HepG2 cells. Data from the lab shows that As2O3 induces mitochondrial dependent apoptosis. Thiorendoxin-1 acts as an important redox homeostasis factor, so, by mutating the molecule, the drug is able to induce cell destruction. When trying to alter the TRX1 protein using RNA interference, the look into crowd discovered that by treatment of Ti214-transfected HepG2 cells with As2O3 resulted in a solid increase of apoptosis compared with untreated control cells. The research group also found that, by constructing recombinant adenovir functions expressing the wild-type TRX1 and mutant TRX1, when over-expressing the TRX1, drug-induced apoptosis is inhibited. The experiments were performed with cautiously so that the info from the result was accurate. All of ! the experiments were tested on multiple take ins under akin conditions on convertible samples with control. During the experiment the cell deaths were counted by staining the cells with Hoechst 33342 and observing the sample under a florescent microscope, allowing the research group to collect the selective information on number of apoptotic cells. Western Blotting and other technique were use in the experiment to accurately identify the protein. Also, statistical analysis was used to determine the significant difference with value P

No comments:

Post a Comment