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

Essay by poppinbeastHigh School, 11th gradeA+, April 2008

download word file, 2 pages 0.0

Downloaded 393 times

Redox status of thioredoxin-1 (TRX1) determines the sensitivity of human liver carcinoma cells (HepG2) to arsenic trioxide-induced cell deathScientific 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 tested the role of thiorendoxin-1 (TRX1) in inducing apoptosis, self-destruction of the cell, using arsenic trioxide (As2O3) in a HepG2 cell. Inducing apoptosis, by using arsenic trioxide and inhibiting TRX1 proteins in cancer cells can be very helpful in reducing the growth of cancerous cells and saving a number of lives. The experiments were conducted by the researching team to test the function of thiorendoxin-1.

The results of the experiment show that the by inactivation of the TRX1 molecule, either by mutation of the active site or oxidation, As2O3 can induce mitochondrial dependent apoptosis.

The lab group tested thiorendoxin-1 in HepG2 cells and it proved that thiorendoxin-1 had an important 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 research group discovered that by treatment of Ti214-transfected HepG2 cells with As2O3 resulted in a significant increase of apoptosis compared with untreated control cells. The research group also found that, by constructing recombinant adenoviruses 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 data from the result was accurate.

All of the experiments were tested on multiple samples under similar conditions on similar 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 data on number of apoptotic cells. Western Blotting and other technique were used in the experiment to accurately identify the protein. Also, statistical analysis was used to determine the significant difference with value P<0.05 considered significant. The constants of the experiment make it possible for the data to be comparable to each other and to allow the group to accurately conclude the claim.

The researchers’ experiment could allow scientists to advance and/or improve the current treatment for cancer, and improve the conditions in which the patient is treated under. Due to the research, TRX1 can be manipulated in cancerous cells to induce apoptosis of the cells and reduce the tumor mass. The results of the experiment can clarify many cancerous cell related dilemmas and help cure cancer.

My reaction to the article was hopeful because it was very ensuring to know that scientist are still making much progress in the study of cancer, helping improve many of the current treatment. Although reading the article was very confusing and tedious work, it told me what was expected of me if I was to become a scientist and what to expect from the job for myself.

Work Cited: Changhai Tian, Ping Gao, Yanhua Zheng, Wen Yue, Xiaohui Wang, Haijing Jin and Quan Chen. “Redox status of thioredoxin-1 (TRX1) determines the sensitivity of human liver carcinoma cells (HepG2) to arsenic trioxide-induced cell death”. NATURE. 1999