We are analyzing https://link.springer.com/article/10.1007/s10549-011-1604-1.

Title:
MiR-28 regulates Nrf2 expression through a Keap1-independent mechanism | Breast Cancer Research and Treatment
Description:
NF-E2-related factor 2 (Nrf2) is an important transcription factor involved in antioxidant response. Nrf2 binds antioxidant response elements (ARE) within promoters of genes encoding detoxification enzymes (e.g., NAD (P) H-quinone oxidoreductase 1 (NQO1)) leading to their transcriptional activation. Nrf2 function is regulated post-translationally by its negative regulator Kelch-like ECH-associated protein 1 (Keap1) that binds Nrf2 and induces cytoplasmic Nrf2 degradation. Our present studies provide new evidence that Nrf2 expression can be regulated by a Keap1-independent mechanism. Here, we utilized breast epithelial cells to explore the impact of microRNA (miRNA) on Nrf2 expression. We found that Nrf2 mRNA levels are reversibly correlated with miR-28 expression and that ectopic expression of miR-28 alone reduces Nrf2 mRNA and protein levels. We further investigated the molecular mechanisms by which miR-28 inhibits Nrf2 mRNA expression. Initially, the ability of miR-28 to regulate the 3′ untranslated region (3′UTR) of Nrf2 mRNA was evaluated via luciferase reporter assay. We observed that miR-28 reduces wild-type Nrf2 3′UTR luciferase reporter activity and this repression is eliminated upon mutation of the miR-28 targeting seed sequence within the Nrf2 3′UTR. Moreover, over-expression of miR-28 decreased endogenous Nrf2 mRNA and protein expression. We also explored the impact of miR-28 on Keap1-Nrf2 interactions and found that miR-28 over-expression does not alter Keap1 protein levels and has no effect on the interaction of Keap1 and Nrf2. Our findings, that miR-28 targets the 3′UTR of Nrf2 mRNA and decreases Nrf2 expression, suggest that this miRNA is involved in the regulation of Nrf2 expression in breast epithelial cells.
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Keywords {🔍}

article, google, scholar, pubmed, cas, nrf, cancer, expression, cell, breast, keap, regulation, biol, protein, research, factor, mrna, transcription, cells, microrna, carcinogenesis, usa, res, oxidative, stress, micrornas, privacy, cookies, response, enzymes, mice, signaling, content, publish, search, yao, zhang, zhou, antioxidant, mechanisms, utr, targeting, access, glutathione, increased, proc, natl, acad, sci, phase,

Topics {✒️}

nf-e2 p45-related factor yongshu zhang & qun zhou month download article/chapter mirna-mediated gene silencing small-cell lung cancer ii drug-metabolizing enzymes luciferase reporter assay breast epithelial cells transcription factor nrf2 antioxidant response element dysfunctional keap1-nrf2 interaction reduces nrf2 mrna cancer stem cells full article pdf glutathione biosynthetic enzymes androgen receptor mrna privacy choices/manage cookies targeting nrf2 signaling microrna biogenesis pathways ]pyrene-dna adducts estrogen signaling activates keap1-independent mechanism targeting carcinogen metabolism nrf2 mrna levels qun zhou keap1-nrf2 interactions sickle cell disease squammous cell carcinoma keap1 sensor modified cancer chemopreventive agents european economic area h-quinone oxidoreductase 1 negative regulator kelch present studies provide nucleic acid alkylation double-edged sword dinkova-kostova reactive oxygen species ectodermal-neural cortex 1 micro-rna profiling cullin 3-roc1 ligase increased protein stability actively translating polyribosomes article yang nrf2-keap1 regulation decreases nrf2 expression increased cell migration conditions privacy policy antioxidant response regulated post-translationally

Questions {❓}

Filipowicz W, Bhattacharyya S, Sonenberg N (2008) Mechanisms of post-transcriptional regulation by microRNAs: are the answers in sight?
Kensler T, Wakabayashi N (2010) Nrf2: friend or foe for chemoprevention?

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         description:NF-E2-related factor 2 (Nrf2) is an important transcription factor involved in antioxidant response. Nrf2 binds antioxidant response elements (ARE) within promoters of genes encoding detoxification enzymes (e.g., NAD (P) H-quinone oxidoreductase 1 (NQO1)) leading to their transcriptional activation. Nrf2 function is regulated post-translationally by its negative regulator Kelch-like ECH-associated protein 1 (Keap1) that binds Nrf2 and induces cytoplasmic Nrf2 degradation. Our present studies provide new evidence that Nrf2 expression can be regulated by a Keap1-independent mechanism. Here, we utilized breast epithelial cells to explore the impact of microRNA (miRNA) on Nrf2 expression. We found that Nrf2 mRNA levels are reversibly correlated with miR-28 expression and that ectopic expression of miR-28 alone reduces Nrf2 mRNA and protein levels. We further investigated the molecular mechanisms by which miR-28 inhibits Nrf2 mRNA expression. Initially, the ability of miR-28 to regulate the 3′ untranslated region (3′UTR) of Nrf2 mRNA was evaluated via luciferase reporter assay. We observed that miR-28 reduces wild-type Nrf2 3′UTR luciferase reporter activity and this repression is eliminated upon mutation of the miR-28 targeting seed sequence within the Nrf2 3′UTR. Moreover, over-expression of miR-28 decreased endogenous Nrf2 mRNA and protein expression. We also explored the impact of miR-28 on Keap1-Nrf2 interactions and found that miR-28 over-expression does not alter Keap1 protein levels and has no effect on the interaction of Keap1 and Nrf2. Our findings, that miR-28 targets the 3′UTR of Nrf2 mRNA and decreases Nrf2 expression, suggest that this miRNA is involved in the regulation of Nrf2 expression in breast epithelial cells.
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