Impact of nuclear factor erythroid-derived 2–like 2 and p62/sequestosome expression on prognosis of patients with gliomas

Zhao, Mingfei; Xu, Hui; Zhang, Buyi; Hong, Bo; Yan, Wei; Zhang, Jianmin

doi:10.1016/j.humpath.2015.02.009

Cited by 32 publications

(19 citation statements)

References 34 publications

(45 reference statements)

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“…Second, p62 gene contain an ARE (antioxidant response element) in its promoter, which is a specific Nrf2‐binding site by which Nrf2 induces p62 transcription . Moreover, Nrf2 and p62 were upregulated in some cancers such as liver cancer , gliomas , ovarian cancer , and breast cancer . In this study, we confirmed that Nrf2 and p62 were overexpressed and there was a positive correlation between them in breast cancer tissues and cells.…”

Section: Discussionsupporting

confidence: 71%

PA‐MSHA inhibits the growth of doxorubicin‐resistant MCF‐7/ADR human breast cancer cells by downregulating Nrf2/p62

et al. 2016

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Acquired resistance to doxorubicin in breast cancer is a serious therapeutic problem. In this study, we investigated whether Pseudomonas aeruginosa mannose‐sensitive hemagglutinin (PA‐MSHA) could inhibit the growth of doxorubicin‐resistant breast cancer cells. We found that the expressions of Nrf2 and p62 in breast cancer were higher than that in the corresponding adjacent normal tissues and benign breast epithelial cell. The expressions of Nrf2 and p62 in breast cancer doxorubicin‐resistant cells MCF‐7/ADR were higher than that in doxorubicin‐sensitive cells MCF‐7. Silencing of Nrf2 or p62 rendered breast cancer cells more susceptible to doxorubicin. We further demonstrated that PA‐MSHA inhibited growth and induced apoptosis of MCF‐7/ADR cells but not MCF‐7 cells. Subcutaneous administration of PA‐MSHA greatly inhibited the growth of xenograft tumors from MCF‐7/ADR cells in nude mice. In addition, PA‐MSHA could downregulate Nrf2 and p62 in vitro and in vivo. These results suggested that activation of Nrf2 and p62 was associated with doxorubicin resistance in breast cancer. PA‐MSHA could inhibit the growth of doxorubicin‐resistant MCF‐7/ADR cells and its potential mechanism might be due to the suppression of Nrf2/p62. It indicated the possibility of using PA‐MSHA in doxorubicin‐resistant breast cancer.

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Section: Discussionsupporting

confidence: 71%

PA‐MSHA inhibits the growth of doxorubicin‐resistant MCF‐7/ADR human breast cancer cells by downregulating Nrf2/p62

et al. 2016

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“…On the other hand, CHQ leads to the accumulation of a multifunctional protein chaperone p62 (also known as sequestome-1, SQSTM-1), whose expression is associated with increased cell proliferation, tumor growth and cytotoxic resistance in different types of human cancers (65). In gliomas, p62 expression correlates with the tumor grade and shorter survival (66, 67). As p62 is an autophagy adaptor targeted for degradation through autophagic clearance, autophagy inhibition by CHQ leads to the increase of the p62 protein levels (68).…”

Section: Functional Pleiotropy Of Chloroquine: the Balance Of Good Anmentioning

confidence: 99%

Re-purposing Chloroquine for Glioblastoma: Potential Merits and Confounding Variables

2018

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There is a growing evidence that antimalarial chloroquine could be re-purposed for cancer treatment. A dozen of clinical trials have been initiated within the past 10 years to test the potential of chloroquine as an adjuvant treatment for therapy–refractory cancers including glioblastoma, one of the most aggressive human cancers. While there is considerable evidence for the efficacy and safety of chloroquine the mechanisms underlying the tumor suppressive actions of this drug remain elusive. Up until recently, inhibition of the late stage of autophagy was thought to be the major mechanism of chloroquine-mediated cancer cells death. However, recent research provided compelling evidence that autophagy-inhibiting activities of chloroquine are dispensable for its ability to suppress tumor cells growth. These unexpected findings necessitate a further elucidation of the molecular mechanisms that are essential for anti-cancer activities of CHQ. This review discusses the versatile actions of chloroquine in cancer cells with particular focus on glioma cells.

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“…Also, higher expression of this subunit was found in glioma patients, and was associated with glutamate excitotoxicity, induced seizures and worse prognosis (Robert et al, 2015). Interestingly, there is a positive correlation between overexpression of Nrf2, tumor grade and reduced survival in patients with glioma (Zhao et al, 2015). It has been proposed that in basal conditions, Nrf1 negatively regulates cysteine/glutamate antiporter system x c -, but in the presence of oxidative stress, Nrf2 is recruited to the ARE sequence in the promoter of the gene and activates its transcription (Tsujita et al, 2014).…”

Section: Slc Transportersmentioning

confidence: 99%

Nrf2 activation in the treatment of neurodegenerative diseases: a focus on its role in mitochondrial bioenergetics and function

Esteras¹,

Dinkova‐Kostova²,

Abramov³

2016

Biological Chemistry

139

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Abstract:The nuclear factor erythroid-derived 2 (NF-E2)-related factor 2 (Nrf2) is a transcription factor wellknown for its function in controlling the basal and inducible expression of a variety of antioxidant and detoxifying enzymes. As part of its cytoprotective activity, increasing evidence supports its role in metabolism and mitochondrial bioenergetics and function. Neurodegenerative diseases are excellent candidates for Nrf2-targeted treatments. Most neurodegenerative conditions such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, frontotemporal dementia and Friedreich's ataxia are characterized by oxidative stress, misfolded protein aggregates, and chronic inflammation, the common targets of Nrf2 therapeutic strategies. Together with them, mitochondrial dysfunction is implicated in the pathogenesis of most neurodegenerative disorders. The recently recognized ability of Nrf2 to regulate intermediary metabolism and mitochondrial function makes Nrf2 activation an attractive and comprehensive strategy for the treatment of neurodegenerative disorders. This review aims to focus on the potential therapeutic role of Nrf2 activation in neurodegeneration, with special emphasis on mitochondrial bioenergetics and function, metabolism and the role of transporters, all of which collectively contribute to the cytoprotective activity of this transcription factor.

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Impact of nuclear factor erythroid-derived 2–like 2 and p62/sequestosome expression on prognosis of patients with gliomas

Cited by 32 publications

References 34 publications

PA‐MSHA inhibits the growth of doxorubicin‐resistant MCF‐7/ADR human breast cancer cells by downregulating Nrf2/p62

PA‐MSHA inhibits the growth of doxorubicin‐resistant MCF‐7/ADR human breast cancer cells by downregulating Nrf2/p62

Re-purposing Chloroquine for Glioblastoma: Potential Merits and Confounding Variables

Nrf2 activation in the treatment of neurodegenerative diseases: a focus on its role in mitochondrial bioenergetics and function

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