Correction for: Ubiquitin-specific protease 4 promotes metastasis of hepatocellular carcinoma by increasing TGF-β signaling-induced epithelial-mesenchymal transition

Qiu, Chao; Liu, Yan; Mei, Ying; Zou, Min; Zhang, Zhibo; Ye, Mingxin; Wu, Xiaoling

doi:10.18632/aging.102010

Cited by 3 publications

(2 citation statements)

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“…To determine the levels of proteins, Western blot was performed as previously described. 32 Primary antibodies against BRD4, Keap1, Nrf2, Histone H3, and GAPDH (Abcam, Cambridge, UK) were utilized in the experiments. Proteins were developed by a horseradish peroxidase-conjugated secondary antibody (Abcam) and ECL Plus Western Blotting Substrate (Thermo Fisher Scientific, Waltham, MA, USA).…”

Section: Protein Extraction and Western Blotmentioning

confidence: 99%

Suppression of bromodomain-containing protein 4 protects trophoblast cells from oxidative stress injury by enhancing Nrf2 activation

Zhang

et al. 2020

Hum Exp Toxicol

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Oxidative stress is considered a key hallmark of preeclampsia, which causes the dysregulation of trophoblast cells, and it contributes to the pathogenesis of preeclampsia. Emerging evidence has suggested bromodomain-containing protein 4 (BRD4) as a key regulator of oxidative stress in multiple cell types. However, whether BRD4 participates in regulating oxidative stress in trophoblast cells remains undetermined. The current study was designed to explore the potential function of BRD4 in the regulation of oxidative stress in trophoblast cells. Our data revealed that BRD4 expression was elevated in trophoblast cells stimulated with hydrogen peroxide. Exposure to hydrogen peroxide caused marked decreases in the levels of proliferation and invasion but promoted apoptosis and the production of ROS in trophoblast cells. Knockdown of BRD4, or treatment with a BRD4 inhibitor, markedly increased the levels of cell proliferation and invasion and decreased apoptosis and ROS production following the hydrogen peroxide challenge. Further data indicated that suppression of BRD4 markedly decreased the expression levels of Keap1, but increased the nuclear expression of Nrf2 and enhanced Nrf2-mediated transcriptional activity. BRD4 inhibition-mediated protective effects were markedly reversed by Keap1 overexpression or Nrf2 inhibition. Overall, these results demonstrated that BRD4 inhibition attenuated hydrogen peroxide-induced oxidative stress injury in trophoblast cells by enhancing Nrf2 activation via the downregulation of Keap1. Our study highlights the potential importance of the BRD4/Keap1/Nrf2 axis in the modulation of the oxidative stress response in trophoblast cells. Targeted inhibition of BRD4 may offer new opportunities for the development of innovative therapeutic approaches to treat preeclampsia.

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Section: Protein Extraction and Western Blotmentioning

confidence: 99%

Suppression of bromodomain-containing protein 4 protects trophoblast cells from oxidative stress injury by enhancing Nrf2 activation

Zhang

et al. 2020

Hum Exp Toxicol

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“…A direct interaction of USP4 with TβRI mediates deubiquitylation and stabilization of TβRI at the plasma membrane, and regulates activity status of TGF-β transduction pathways [10][11]. Some previous studies showed that USP4 is aberrantly expressed and might act as an oncogene in multiple types of cancer, such as in human sarcoma, colorectal cancer, hepatocellular carcinoma and breast cancer [12][13][14][15][16][17][18]. Peter et al find out that USP4 can facilitate development of TGF-β-induced EMT in vitro in breast cancer cells [19].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of USP4 attenuates epithelial-mesenchymal transition of renal tubular epithelial cells by TβRI

Zhang

Wang

et al. 2020

Preprint

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Objective We aimed to explore the role of ubiquitin-specific peptidase-4 (USP4) in TGF-β1 induced epithelial-mesenchymal transition (EMT) during renal fibrosis, and investigated that if Akt inactivation exerted a critical effect on EMT via USP4/TβRI pathway. Methods USP4, pAkt and TβRI proteins in the obstructed kidneys from unilateral ureteral obstruction (UUO) rats were detected by immunohistochemistry assay or western blot method. E-cadherin, α-SMA, USP4 and pAkt protein expression in NRK-52E cells at different concentration of TGF-β1 were detected at different time. Further, NRK-52E cells were transfected with USP4-specific siRNA (si-USP4), and then stimulated with 10 ng/ml TGF-β1 for 24h to detect E-cadherin, α-SMA, E-cadherin and TβRI by immunofluorescent double staining assay. Pretreated with PI3K inhibitor LY294002, protein expression levels of pAkt, E-cadherin, α-SMA were detected. Meanwhile, the location of USP4 was visualized by immunofluorescent assay in NRK-52E cells. Results The expression of USP4 and TβRI was significantly upregulated in the tubular epithelial cells of UUO rats. We also found that TGF-β1 upregulated USP4 and activated Akt in NRK-52E cells during EMT. In vitro, downregulation of USP4 inhibited TβRI expression and partially reversed EMT stimulated by TGF-β1. In the meantime, blunted phosphorylation of Akt with LY294002 promoted the E-cadherin expression, and inhibited α-SMA expression in response to TGF-β1. However, inactivation of Akt could reverse EMT process, but failed to induce USP4 to shuttle between the nucleus and the cytoplasm in NRK-52E cells stimulated by TGF-β1. Conclusions These data implied that USP4 was a harmful molecule induced by TGF-β1, regulated by Akt activation and promoted TGF-β1-induced EMT via TβRI in tubular epithelial cells during renal fibrosis.

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Pro-apoptotic and anti-apoptotic regulation mediated by deubiquitinating enzymes

Choi

Baek

2022

Cell. Mol. Life Sci.

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Correction for: Ubiquitin-specific protease 4 promotes metastasis of hepatocellular carcinoma by increasing TGF-β signaling-induced epithelial-mesenchymal transition

Cited by 3 publications

References 0 publications

Suppression of bromodomain-containing protein 4 protects trophoblast cells from oxidative stress injury by enhancing Nrf2 activation

Suppression of bromodomain-containing protein 4 protects trophoblast cells from oxidative stress injury by enhancing Nrf2 activation

Inhibition of USP4 attenuates epithelial-mesenchymal transition of renal tubular epithelial cells by TβRI

Pro-apoptotic and anti-apoptotic regulation mediated by deubiquitinating enzymes

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