2010
DOI: 10.1016/j.abb.2010.05.012
|View full text |Cite
|
Sign up to set email alerts
|

Glutathione transferases and development of new principles to overcome drug resistance

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1
1

Citation Types

4
198
0
5

Year Published

2011
2011
2022
2022

Publication Types

Select...
8
1

Relationship

1
8

Authors

Journals

citations
Cited by 227 publications
(207 citation statements)
references
References 66 publications
4
198
0
5
Order By: Relevance
“…Intrinsic mechanisms of drug resistance are various: induction of efflux transport proteins (ABC proteins, P-glycoprotein), enhancement of DNA repair, maintenance of cells in a predominantly non-cycling state, protection from induced apoptosis and overexpression of detoxification systems, like glutathione transferases (12,(25)(26)(27)(28). In contrast to those cellular mechanisms the extrinsic resistance is dependent on tumour structure, with regions of hypoxia and acidosis, on vascularisation due to the release of pro-angiogenic factors and nutrition supply (29).…”
Section: Discussionmentioning
confidence: 99%
“…Intrinsic mechanisms of drug resistance are various: induction of efflux transport proteins (ABC proteins, P-glycoprotein), enhancement of DNA repair, maintenance of cells in a predominantly non-cycling state, protection from induced apoptosis and overexpression of detoxification systems, like glutathione transferases (12,(25)(26)(27)(28). In contrast to those cellular mechanisms the extrinsic resistance is dependent on tumour structure, with regions of hypoxia and acidosis, on vascularisation due to the release of pro-angiogenic factors and nutrition supply (29).…”
Section: Discussionmentioning
confidence: 99%
“…In the series of compounds bearing an aromatic moiety inserted in the NBD C4-side chain (2e24), the introduction of the phenyl ring directly linked to the sulfur atom (2), and further substituted with polar groups, such as carboxy (6e8), carbethoxy (9) and carboxamido (10e17), led to compounds with 4-fold higher to 4-fold lower potency than 1 against GSTP1-1 (IC 50 values ranging from 0.2 to 3.1 mM), and with highly decreased affinity against GSTM2-2 (IC 50 values from 0.02 to >1 mM, up to 107-fold lower potency than 1). In particular, the benzamide 10, the N-((tetrahydro-2H-pyran-2-yl)oxy)benzamide 14 and the N-(2-(dimethylamino)ethyl)benzamide 17 showed the same or slightly lower GSTP1-1 inhibition than 1, and were much less (20-to 75-folds) effective towards GSTM2-2, thus displaying a selectivity index (SI, IC 50…”
Section: Inhibition Of Gstp1-1 and Gstm2-2mentioning
confidence: 99%
“…Of these, TLK-286 is a promising compound tested in Phase III clinical trials for ovarian cancers [14] and NBDHEX is a compound that may block interactions of GST P1-1 with c-Jun N-terminal kinase (JNK). However, additional inhibitors are in demand, since the toxicity of the known compounds limits their use in clinical and in vitro studies [13]. In the present study the inhibitory effects of a series of novel compounds containing benzothiazole and benzoxazole groups were studied with human GST P1-1.…”
Section: Introductionmentioning
confidence: 99%
“…A variety of compounds can be identified in the literature as inhibitors of GST P1-1. Ethacrynic acid, TLK-286, 6-(7-nitro-1,2,3-benzoxadiazol-4-ylthio) hexanol (NBDHEX), Cibacron blue and bromosulfophthalein are known amongst the most potent ones [3,13]. Of these, TLK-286 is a promising compound tested in Phase III clinical trials for ovarian cancers [14] and NBDHEX is a compound that may block interactions of GST P1-1 with c-Jun N-terminal kinase (JNK).…”
Section: Introductionmentioning
confidence: 99%