C/EBPβ regulates sensitivity to bortezomib in prostate cancer cells by inducing REDD1 and autophagosome–lysosome fusion

Barakat, David J.; Mendonca, Janet; Barberi, Theresa J.; Zhang, Jing; Kachhap, Sushant K.; Paz‐Priel, Ido; Friedman, Alan D.

doi:10.1016/j.canlet.2016.03.005

Cited by 30 publications

(27 citation statements)

References 56 publications

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“…ÃÃÃÃ , P < 0.0001; ÃÃÃ , P < 0.001; ÃÃ , P < 0.01; Ã , P < 0.05. (14) and prostate cancer cells (15). In this experiment, Taxol doses at IC 25 concentrations had no obvious effect on autophagy or REDD1 expression in T24 and RT4 cells (data not presented).…”

Section: Discussionmentioning

confidence: 67%

“…Both REDD1 and miR-22 have been reported to participate in regulating the chemosensitivity in a variety of cancers (15,22,27,28). However their roles in Taxol-induced cytotoxity in BUC remain unknown.…”

Section: Involvement Of Redd1 and Mir-22 In Taxol Chemosensitivity Ofmentioning

confidence: 99%

“…REDD1 participates in autophagy induction through the mTOR-EEF2K pathway (13). It has been reported that REDD1-induced autophagy promotes development of drug resistance in myeloma cells (14), and prostate cancer cells (15). As an inhibitor of the mTOR pathway, REDD1 is involved in the regulation of cell growth, tumorigenesis, and cell aging (16,17).…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of REDD1 Sensitizes Bladder Urothelial Carcinoma to Paclitaxel by Inhibiting Autophagy

Zeng

Liu

Cao

et al. 2018

Clinical Cancer Research

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Regulated in development and DNA damage response-1 (REDD1) is a stress-related protein and is involved in the progression of cancer. The role and regulatory mechanism of REDD1 in bladder urothelial carcinoma (BUC), however, is yet unidentified. The expression of REDD1 in BUC was detected by Western blot analysis and immunohistochemistry (IHC). The correlation between REDD1 expression and clinical features in patients with BUC were assessed. The effects of REDD1 on cellular proliferation, apoptosis, autophagy, and paclitaxel sensitivity were determined both and Then the targeted-regulating mechanism of REDD1 by miRNAs was explored. Here the significant increase of REDD1 expression is detected in BUC tissue, and REDD1 is first reported as an independent prognostic factor in patients with BUC. Silencing REDD1 expression in T24 and EJ cells decreased cell proliferation, increased apoptosis, and decreased autophagy, whereas the ectopic expression of REDD1 in RT4 and BIU87 cells had the opposite effect. In addition, the REDD1-mediated proliferation, apoptosis, and autophagy are found to be negatively regulated by miR-22 , which intensify the paclitaxel sensitivity via inhibition of the well-acknowledged REDD1-EEF2K-autophagy axis. AKT/mTOR signaling initially activated or inhibited in response to silencing or enhancing REDD1 expression and then recovered rapidly. Finally, the inhibited REDD1 expression by either RNAi or miR-22 sensitizes BUC tumor cells to paclitaxel in a subcutaneous transplant carcinoma model REDD1 is confirmed as an oncogene in BUC, and antagonizing REDD1 could be a potential therapeutic strategy to sensitize BUC cells to paclitaxel. .

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Section: Discussionmentioning

confidence: 67%

Section: Involvement Of Redd1 and Mir-22 In Taxol Chemosensitivity Ofmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Inhibition of REDD1 Sensitizes Bladder Urothelial Carcinoma to Paclitaxel by Inhibiting Autophagy

Zeng

Liu

Cao

et al. 2018

Clinical Cancer Research

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“…C/EBPb is also closely related to autophagy by inducing autophagy rhythms in zebrafish and mice through controlling the transcription of autophagy-related genes (51). C/EBPb, a critical effector of autophagy via regulation of autolysosome formation, promotes resistance to proteasome inhibitor treatment (52). These works indicate that C/EBPb may play a role in Meth-induced neuronal apoptosis and autophagy.…”

mentioning

confidence: 89%

Methamphetamine exposure triggers apoptosis and autophagy in neuronal cells by activating the C/EBPβ‐related signaling pathway

Huang

Luo

et al. 2018

The FASEB Journal

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Methamphetamine (Meth) is a widely abused psychoactive drug that primarily damages the nervous system, notably causing dopaminergic neuronal apoptosis. CCAAT-enhancer binding protein (C/EBPβ) is a transcription factor and an important regulator of cell apoptosis and autophagy. Insulin-like growth factor binding protein (IGFBP5) is a proapoptotic factor that mediates Meth-induced neuronal apoptosis, and Trib3 (tribbles pseudokinase 3) is an endoplasmic reticulum (ER) stress-inducible gene involved in autophagic cell death through the mammalian target of rapamycin (mTOR) signaling pathway. To test the hypothesis that C/EBPβ is involved in Meth-induced IGFBP5-mediated neuronal apoptosis and Trib3-mediated neuronal autophagy, we measured the protein expression of C/EBPβ after Meth exposure and evaluated the effects of silencing C/EBPβ, IGFBP5, or Trib3 on Meth-induced apoptosis and autophagy in neuronal cells and in the rat striatum after intrastriatal Meth injection. We found that, at relatively high doses, Meth exposure increased C/EBPβ protein expression, which was accompanied by increased neuronal apoptosis and autophagy; triggered the IGFBP5-mediated, p53-up-regulated modulator of apoptosis (PUMA)-related mitochondrial apoptotic signaling pathway; and stimulated the Trib3-mediated ER stress signaling pathway through the Akt-mTOR signaling axis. We also found that autophagy is an early response to Meth-induced stress upstream of apoptosis and plays a detrimental role in Meth-induced neuronal cell death. These results suggest that Meth exposure induces C/EBPβ expression, which plays an essential role in the neuronal apoptosis and autophagy induced by relatively high doses of Meth; however, relatively low concentrations of Meth did not change the expression of C/EBPβ in vitro. Further studies are needed to elucidate the role of C/EBPβ in low-dose Meth-induced neurotoxicity.-Xu, X., Huang, E., Luo, B., Cai, D., Zhao, X., Luo, Q., Jin, Y., Chen, L., Wang, Q., Liu, C., Lin, Z., Xie, W.-B., Wang, H. Methamphetamine exposure triggers apoptosis and autophagy in neuronal cells by activating the C/EBPβ-related signaling pathway.

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“…Although BTZ maintains superiority in cancer treatment, many issues still limit its effectiveness, such as poor solubility, drug resistance and severe side effects. To address those problems and explore the chemotherapy mechanism of BTZ, it is necessary to introduce suitable carriers for delivery of BTZ to targeted cancer regions …”

Section: Introductionmentioning

confidence: 99%

Reduced graphene oxide‐based bortezomib delivery system for photothermal chemotherapy with enhanced therapeutic efficacy

et al. 2018

Polymer International

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In cancer treatment, it still is a curial challenge to enhance therapeutic efficacy and reduce side effects. A novel reduced graphene oxide‐based nanoplatform (rGO/PDex) has been constructed to deliver an anticancer drug, bortezomib (BTZ), for photo‐chemotherapy. The structure and properties of the nanoplatform were characterized. The obtained data strongly indicated that rGO/PDex had enhanced stability. Further, folic acid was introduced and the resulting rGO/PDexF nanoplatform exhibited improved cellular uptake due to the active targeting effect. The anticancer drug BTZ could be effectively encapsulated into the rGO‐based nanoplatform and be released in a controlled manner. In vitro experiments demonstrated that BTZ‐loaded rGO‐based nanoparticles displayed enhanced therapeutic efficacy compared with the single chemotherapy, indicating the great potential of rGO‐based nanoparticles for cancer treatments. © 2018 Society of Chemical Industry

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C/EBPβ regulates sensitivity to bortezomib in prostate cancer cells by inducing REDD1 and autophagosome–lysosome fusion

Cited by 30 publications

References 56 publications

Inhibition of REDD1 Sensitizes Bladder Urothelial Carcinoma to Paclitaxel by Inhibiting Autophagy

Inhibition of REDD1 Sensitizes Bladder Urothelial Carcinoma to Paclitaxel by Inhibiting Autophagy

Methamphetamine exposure triggers apoptosis and autophagy in neuronal cells by activating the C/EBPβ‐related signaling pathway

Reduced graphene oxide‐based bortezomib delivery system for photothermal chemotherapy with enhanced therapeutic efficacy

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