therapeutic approach forNRF2‐addicted cancers andNRF2 inhibitors are being actively developed. However, giving systemicNRF2 inhibitors might have undesirable effects on cancer‐bearing hosts, considering the central roles ofNRF2 in cytoprotection. To avoid these side‐effects, new therapeutic targets besides...
In many human cancer cells, the KEAP1-mediated regulation of NRF2 activity is abrogated, resulting in the persistent activation of NRF2. Persistently activated NRF2 drives malignant progression of cancers by increasing therapeutic resistance and promoting aggressive tumorigenesis, a state termed as NRF2 ...
Multiple lines of evidence suggest that aberrantly activated NRF2 in cancer cells drives their malignant progression and that the cancer cells consequently develop 'NRF2 addiction.' Although the downstream effectors of NRF2 that are responsible for cancer malignancy have been extensively studied, mechanisms...
NRF2 addiction in cancer cells. Cancer Sci. 109, 900–911 (2018). Article CAS PubMed PubMed Central Google Scholar Guo, Q. J. et al. MicroRNA-510 promotes cell and tumor growth by targeting peroxiredoxin1 in breast cancer. Breast Cancer Res. 15, R70 (2013). Article PubMed PubMed ...
自噬受体蛋白p62与Keap1-Nrf2信号通路在肿瘤中的研究进展
cancer cells can hijack NRF2 pathways24 and maintain high activation levels (NRF2 addiction) to ensure a better survival, stronger therapeutic resistance, and more aggressive behavior.13 Such an activation of NRF2 has been proposed in many studies13,25–27 as a prognostic factor for cancer ...
In the context of NRF2-addiction, recent evidence has highlighted various modes of NRF2 inhibition that may serve as targetable cascades to treat this subset of cancers. This is of particular importance as constitutive activation of NRF2 has been shown to enhance resistance to cancer therapies and ...
Other studies in cancer cells implicated a role for TUG1 in drug resistance [49]. TUG1 also has been shown to induce cardiac hypertrophy and diastolic dysfunction in db/db mouse cardiomyocytes [48]. On the other hand, TUG1 was reported to inhibit renal fibrosis in diabetic nephropathy mice ...
We identify melanoma addiction to the mitochondrial protein glutaryl-CoA dehydrogenase (GCDH), which functions in lysine metabolism and controls protein glutarylation. GCDH knockdown induced cell death programmes in melanoma cells, an activity blocked by inhibition of the upstream lysine catabolism enzyme ...
When NRF2 strongly and persistently promotes glutathione synthesis, which often occurs in NRF2-activated cancer cells with KEAP1 mutations [49], mitochondrial cysteine demand may not be satisfied, resulting in mitochondrial suppression. In addition, NRF2-activated cancer cells are subjected to a ...