Abstract:Transitional cell carcinoma (TCC) of urinary bladder belongs to glutathione S-transferase P1 (GSTP1) overexpressing tumors. Upregulated GSTP1 in TCC is related to apoptosis inhibition. This antiapoptotic effects of GSTP1 might be mediated through protein:protein interaction with c-Jun NH2 -terminal kinase (JNK). Herein, we analyzed whether a direct link between GSTP1 and JNK exists in TCC. The presence of GSTP1/JNK complexes was analyzed by immunoprecipitation and Western blotting in 20 TCC specimens, obtained… Show more
“…In TCC, it can be speculated that increased GSTO1 expression through its deglutathionylase activity keeps the GSTP1 in complex with JNK, contributing to the apoptosis resistance. Indeed, the existence of GSTP1: JNK interaction in both TCC 5637 cell line and TCC tumor tissue was confirmed in our earlier investigation [19], while in the current study, we have shown, for the first time, the association between GSTO1 and GSTP1 by immunoprecipitation. Additionally, we have looked for the possible association of GSTO1-1 with some of the signaling molecules of PI3K and MAPK pathways known to be regulated by S-glutathionylation.…”
“…In TCC, it can be speculated that increased GSTO1 expression through its deglutathionylase activity keeps the GSTP1 in complex with JNK, contributing to the apoptosis resistance. Indeed, the existence of GSTP1: JNK interaction in both TCC 5637 cell line and TCC tumor tissue was confirmed in our earlier investigation [19], while in the current study, we have shown, for the first time, the association between GSTO1 and GSTP1 by immunoprecipitation. Additionally, we have looked for the possible association of GSTO1-1 with some of the signaling molecules of PI3K and MAPK pathways known to be regulated by S-glutathionylation.…”
“…Since UC is often associated with exposure to carcinogens, researchers have evaluated the use of the GST genotype for stratifying UC risk (Kempkes et al, 1996). Other studies have investigated either GST genetic polymorphisms or tissue-specific GST expression in bladder cancer (Giralt et al, 1993;Pljesa-Ercegovac et al, 2010;PljesaErcegovac et al, 2011). Although the GST isoenzyme pattern in UC resembles that of the corresponding normal uroepithelium, the increased expressions of all GST subtypes reportedly correspond with progression of the cancer (Simic et al, 2005).…”
Objectives: Glutathione S-transferase (GST) isoenzymes play important roles in resistance to cell apoptosis and carcinogenesis. We aimed to establish the relationship between GST expression and the prognosis of upper urinary tract urothelial carcinoma (UTT-UC) in Taiwan. Methods: This study retrospectively reviewed 46 patients with pathologically confirmed UUT-UC at Kaohsiung Medical University Hospital. In each patient, expression of GSTT1 and GSTP1 was compared between urothelial carcinoma and normal urothelial cells by Western blotting. Results: GSTP1 expression in the UUT-UC cells was significantly higher than that in normal urothelial cells (1.6 fold, p<0.001). Expression of GSTT1 was significantly associated with the invasiveness of the carcinoma (p=0.006). Conclusions: In UUT-UC, GSTP1 might be a potential tumor marker, whereas high GSTT1 expression could be used as an indicator of cancer progression. This study is the first to demonstrate potential applications of different GST isoenzymes for biomolecular analysis of UUT-UCs in Taiwan.
“…The research interest in GSTP1 covers last 22 years with a peak in 2012. GSTP1 widely represented in oncology connecting oxidative stress, apoptosis and carcinogenesis [ 147 , 148 , 149 ], but also plays a role in asthma [ 150 ], Parkinson’s disease [ 151 ]. Kidney damage was also reported in conjunction, however much less supported [ 151 ].…”
Section: Regulatory Pathways and Antioxidative Therapiesmentioning
Oxidative stress is an imbalance between pro- and antioxidants that adversely influences the organism in various mechanisms and on many levels. Oxidative damage occurring concomitantly in many cellular structures may cause a deterioration of function, including apoptosis and necrosis. The damage leaves a molecular “footprint”, which can be detected by specific methodology, using certain oxidative stress biomarkers. There is an intimate relationship between oxidative stress, inflammation, and functional impairment, resulting in various diseases affecting the entire human body. In the current narrative review, we strengthen the connection between oxidative stress mechanisms and their active compounds, emphasizing kidney damage and renal transplantation. An analysis of reactive oxygen species (ROS), antioxidants, products of peroxidation, and finally signaling pathways gives a lot of promising data that potentially will modify cell responses on many levels, including gene expression. Oxidative damage, stress, and ROS are still intensively exploited research subjects. We discuss compounds mentioned earlier as biomarkers of oxidative stress and present their role documented during the last 20 years of research. The following keywords and MeSH terms were used in the search: oxidative stress, kidney, transplantation, ischemia-reperfusion injury, IRI, biomarkers, peroxidation, and treatment.
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