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Inhibition of the Nrf2-TrxR Axis Sensitizes the Drug-Resistant Chronic Myelogenous Leukemia Cell Line K562/G01 to Imatinib Treatments.
Abstract Nuclear factor erythroid 2-related factor 2 (Nrf2) is involved in tumor drug resistance, but its role in imatinib resistance of chronic myeloid leukemia (CML) remains elusive. We aimed to investigate the effects of Nrf2 on drug sensitivity, thioredoxin reductase (TrxR) expression, reactive oxygen species (ROS) production, and apoptosis induction in imatinib-resistant CML K562/G01 cells and explored their potential mechanisms. Stable K562/G01 cells with knockdown of Nrf2 were established by infection of siRNA-expressing lentivirus. The mRNA and protein expression levels of Nrf2 and TrxR were determined by ...
Source: Biomed Res - December 14, 2019 Category: Research Authors: Xu L, Zhao Y, Pan F, Zhu M, Yao L, Liu Y, Feng J, Xiong J, Chen X, Ren F, Tan Y, Wang H Tags: Biomed Res Int Source Type: research

CCDC26 knockdown enhances resistance of gastrointestinal stromal tumor cells to imatinib by interacting with c-KIT.
Authors: Cao K, Li M, Miao J, Lu X, Kang X, Zhu H, Du S, Li X, Zhang Q, Guan W, Dong Y, Xia X Abstract Accumulating evidence indicates that long noncoding RNAs (lncRNAs) are involved in diseases such as cancer. However, little is known about the role of lncRNAs in gastrointestinal stromal tumors (GIST). In the present study, we explored the biological function of the lncRNA coiled-coil domain-containing 26 (CCDC26) in imatinib resistance of GIST. We found that human GIST-882 cells with lower CCDC26 expression were less sensitive to imatinib compared with GIST-T1 cells with higher CCDC26 expression. CCDC26 expressio...
Source: American Journal of Translational Research - February 11, 2018 Category: Research Tags: Am J Transl Res Source Type: research

Id: 109: parkin mediates endothelial pro-inflammatory responses in acute lung injury
Conclusion These results suggest that endothelial parkin mediates EC activation and neutrophil adhesion/migration after LPS, and therefore it may represent a new potential therapeutic target in ALI/ARDS.
Source: Journal of Investigative Medicine - March 21, 2016 Category: Research Authors: Letsiou, E., Wang, H., Belvitch, P., Dudek, S., Sammani, S. Tags: Pulmonary/Critical Care Source Type: research

Id: 124: abl family kinases mediate lung vascular permeability and inflammation in acute lung injury
Conclusions The Abl family kinases c-Abl and Arg play complementary but distinct roles in mediating vascular permeability and inflammation following LPS challenge. The promoter of Abl1 (c-Abl) contains antioxidant response elements and LPS causes an increase in c-Abl expression. Additionally, LPS increases the mRNA expression of c-Abl, but not Arg. C-Abl contributes to LPS-induced NFB signaling; whereas Arg contributes to inter-endothelial gap formation and adherens junction stability. Inhibition of both of these kinases may be of benefit in patients with ARDS.
Source: Journal of Investigative Medicine - March 21, 2016 Category: Research Authors: Rizzo, A., Letsiou, E., Dudek, S., Sun, X., Garcia, J. Tags: Pulmonary/Critical Care Source Type: research

A combination of STI571 and BCR-ABL1 siRNA with overexpressed p15INK4B induced enhanced proliferation inhibition and apoptosis in chronic myeloid leukemia.
In conclusion, our study may provide new insights into the role of p15INK4B in CML and a potential therapeutic target for overcoming tyrosine kinase inhibitor resistance in CML. PMID: 25387678 [PubMed - in process]
Source: Braz J Med Biol Res - November 16, 2014 Category: Research Authors: Xia DY, Liu L, Hao MW, Liu Q, Chen RA, Liang YM Tags: Braz J Med Biol Res Source Type: research