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FOXO3a protects glioma cells against temozolomide-induced DNA double strand breaks via promotion of bnip3-mediated mitophagy

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中国药理学报（英文版） 2021年第8期42卷 1324-1337页

作者： Chuan He Shan Lu Xuan-zhong Wang Chong-cheng Wang Lei Wang Shi-peng Liang Tian-fei Luo Zhen-chuan Wang Mei-hua Piao Guang-fan Chi Peng-fei Ge Department of Neurosurgery First Hospital of Jilin UniversityChangchun 130021China Research Center of Neuroscience First Hospital of Jilin UniversityChangchun 130021China Research Center of Neuroscience First Hospital of Jilin UniversityChangchun 130021China Department of Neurology First Hospital of Jilin UniversityChangchun 130021China Department of Anesthesiology First hospital of Jilin UniversityChangchun 130021China Key Laboratory of Pathobiology Ministry of EducationJilin UniversityChangchun 130021China

FOXO3a(forkhead box transcription factor 3a)is involved in regulating multiple biological processes in cancer ***3(Bcl-2/adenovirus E1B 19-kDa-interacting protein 3)is a receptor accounting for priming damaged mitochondria for autophagic *** this study we investigated the role of FOXO3a in regulating the sensitivity of glioma cells to temozolomide(TMZ)and its relationship with bnip3-mediated *** showed that TMZ dosage-dependently inhibited the viability of human U87,U251,T98G,LN18 and rat C6 glioma cells with IC50 values of 135.75,128.26,142.65,155.73 and 111.60 μM,*** U87 and U251 cells,TMZ(200 μM)induced DNA double strand breaks(DSBs)and nuclear translocation of apoptosis inducing factor(AIF),which was accompanied by bnip3-mediated mitophagy and FOXO3a accumulation in *** treatment induced intracellular ROS accumulation in U87 and U251 cells via enhancing mitochondrial superoxide,which not only contributed to DNA DSBs and exacerbated mitochondrial dysfunction,but also upregulated FOXO3a *** of FOXO3a aggravated TMZ-induced DNA DSBs and mitochondrial damage,as well as glioma cell *** treatment not only upregulated bnip3 and activated autophagy,but also triggered mitophagy by prompting bnip3 translocation to mitochondria and reinforcing bnip3 interaction with *** of mitophagy by knocking down bnip3 with SiRNA or blocking autophagy with 3MA or bafilomycin A1 exacerbated mitochondrial superoxide and intracellular ROS ***,FOXO3a knockdown inhibited TMZ-induced bnip3 upregulation and autophagy *** addition,we showed that treatment with TMZ(100 mg·kg-1·d-1,ip)for 12 days in C6 cell xenograft mice markedly inhibited tumor growth accompanied by inducing FOXO3a upregulation,oxidative stress and bnip3-mediated mitophagy in tumor *** results demonstrate that FOXO3a attenuates temozolomide-induced DNA double strand breaks in human glioma cells via promoting BNI

关键词： glioma temozolomide DNA double strand break oxidative stress mitochondrial superoxide bnip3 FOXO3a mitophagy 3MA bafilomycin A

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Angelica polysaccharide moderates hypoxia-evoked apoptosis and autophagy in rat neural stem cells by downregulation of bnip3 (Publication with Expression of Concern)

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ARTIFICIAL CELLS NANOMEDICINE AND BIOTECHNOLOGY 2019年第1期47卷 2492-2499页

作者： Xue, Yongzhen Li, Dongmei Zhang, Yige Gao, Hang Li, Hui East Med Dist Linyi Peoples Hosp Dept Childrens Healthcare Linyi Shandong Peoples R China Shandong Prov Coal Linyi Hot Springs Sanat Hosp Dept Internal Med Linyi Shandong Peoples R China Qingdao Univ Dept Med Classe Six Clin Five Year Syst Qingdao Shandong Peoples R China Jining Med Univ Basic Med Coll Class Eight Clin Med Jining Peoples R China Linyi Womens & Childrens Hosp Dept Childrens Rehabil 1 Qinghe South Rd Linyi 276000 Shandong Peoples R China

Neonatal hypoxia-ischemia is a troublesome disease. Angelica polysaccharide (AP) is proved to have antioxidant effects. Our study was performed to confirm the effects of AP in hypoxia-exposed neural stem cells (NSCs). NSCs were pre-treated with AP and then stimulated with hypoxia. Viability of NSCs was examined by Cell Counting Kit-8 assay. Hypoxia-introduced apoptosis was observed by flow cytometry. Essential regulators of mTOR and Notch signalling pathways were examined by Western blot. mRNA expression was accessed using qRT-PCR. Bcl2/adenovirus EIB 19kD-interacting protein 3 (bnip3) was altered by transfection. We noticed that NSCs were sensitive to hypoxia-induced apoptosis and showed decreased viability. Moreover, Beclin and light chain 3-II was upregulated while p62 was downregulated. However, AP reversed all these results. Similarly, hypoxia decreased the phosphorylation of mTOR and p70S6K and Notch1 expression while AP increased the phosphorylation of mTOR and p70S6K as well as the expression of Notch1. bnip3 was upregulated by hypoxia while downregulated by AP. Further experiments demonstrated that overexpression of bnip3 broken all the effects induced by AP shown in cell viability, apoptosis, autophagy and signalling pathways. Collectively, AP alleviated hypoxia-introduced NSCs damages by maintaining cell viability, blocking apoptosis and autophagy via downregulation of bnip3 with the activation of mTOR and Notch signalling pathways.

关键词： Neonatal hypoxia-ischemia angelica polysaccharide bnip3 mTOR Notch

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Upregulation of long noncoding RNA RP4 exacerbates hypoxia injury in cardiomyocytes through regulating miR-939/bnip3/Wnt/β-catenin pathway (Publication with Expression of Concern. See vol. 50, pg. 221, 2022)

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ARTIFICIAL CELLS NANOMEDICINE AND BIOTECHNOLOGY 2019年第1期47卷 3013-3020页

作者： Rong, Jingfeng Xu, Jijie Liu, Qian Wu, Yaoyao Guo, Honglin Mu, Ting Zhou, Hua Chi, Hao Zhengzhou Univ Luoyang Cent Hosp Dept Med Cardiovasc Luoyang Henan Peoples R China Shanghai Univ Tradit Chinese Med Shuguang Hosp Inst Cardiovasc Res Shanghai Peoples R China Shanghai Univ Tradit Chinese Med Shuguang Hosp Dept Cardiovasc Shanghai Peoples R China Shanghai Univ Tradit Chinese Med Shuguang Hosp Dept Cardiothorac Surg 528 Zhangheng Rd Shanghai 201499 Peoples R China

This research planned to dig the impacts and potential principles of long noncoding RNA RP4 onH9c2 cell injury induced by hypoxia. The H9c2 cardiac muscle cells were cultured under 3% O-2 concentration to induce hypoxia injury, followed by detection of RP4 expression. RP4 was then over-expressed and silenced to investigate its effects on cell injury induced by hypoxia. The potential correlation between RP4 and miR-939, between miR-939 and bnip3, and between RP4/miR-939/ bnip3 axis and Wnt/beta-catenin pathway activation were explored. Biological processes (suppressed cell viability, migration and invasion, but enhanced cell apoptosis) were changed by hypoxia. Upregulation of RP4 enhanced hypoxia-produced damage in H9c2 cells. Additionally, miR-939 expression was opposite regulated by RP4, and miR-939 mimic abrogated the influences of pc-RP4 on enhanced hypoxia damage in H9c2 cells. Moreover, bnip3 was targeted by miR-939 and their correlation is negative. Furthermore, upregulation of RP4 exacerbated hypoxia-produced injury in H9c2 cells by sensitizing Wnt/beta-catenin signals in H9c2 cells, which was regulated by miR-939/bnip3 axis. Our findings reveal that RP4 is highly expressed in the hypoxia-resulted H9c2 cells. Enhanced expression of RP4 may exacerbate hypoxia injury in cardiomyocytes through regulating miR-939/bnip3 axis-mediated briskness of Wnt/beta-catenin signals. Our study will offer a fresh theoretical basis for the treatment of ischemic myocardial injury.

关键词： Hypoxia-induced myocardial injury long noncoding RNA RP4 miR-939 bnip3 Wnt/beta-catenin pathway

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Synchronised phosphorylation of bnip3, Bcl-2 and Bcl-xL in response to microtubule-active drugs is JNK-independent and requires a mitotic kinase

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BIOCHEMICAL PHARMACOLOGY 2010年第11期79卷 1562-1572页

作者： Mellor, Howard R. Rouschop, Kasper M. Wigfield, Simon M. Wouters, Bradly G. Harris, Adrian L. Univ Oxford Growth Factor Grp CR UK Mol Oncol Labs John Radcliffe HospWeatherall Inst Mol Med Oxford OX3 9DS England Maastricht Univ Dept Radiat Oncol Maastro Lab GROW Res Inst Maastricht Netherlands Univ Toronto Ontario Canc Inst Univ Hlth Network Dept Radiat Oncol & Med Biophys Toronto ON Canada

bnip3 is a hypoxia-inducible BH3-only member of the Bcl-2 family of proteins that regulate apoptosis and autophagy. However the role of bnip3 in the hypoxia response has proved difficult to define and remains controversial. In this study we show that in cancer cells, knockdown or forced expression of bnip3 fails to modulate cell survival under hypoxic or normoxic conditions. However, we demonstrate that bnip3 is regulated post-translationally, existing as multiple monomeric and dimeric phosphorylated forms. Upon treatment with microtubule inhibitors, but not other classes of chemotherapeutics, bnip3 becomes hyperphosphorylated. We demonstrate that the phosphorylation of bnip3 occurs in synchrony with phosphorylation of its binding partners Bcl-2 and Bcl-xL. Microtubule inhibitor-induced phosphorylation of these proteins occurs independently of the AKT/mTor and JNK kinase pathways and requires Mps1 mitotic checkpoint kinase activity. Inhibition of mitotic arrest in the presence of paclitaxel blocks the phosphorylation of bnip3, Bcl-2 and Bcl-xL, demonstrating that these proteins are phosphorylated by a mitochondrially active mitotic kinase. We show that phosphorylation increases the stability of bnip3 and that bnip3 predominantly interacts with the phosphorylated form of Bcl-2. This study provides new insight into the post-translational functional control of these Bcl-2 family members. (C) 2010 Elsevier Inc. All rights reserved.

关键词： bnip3 Bcl-2 Paclitaxel Phosphorylation Mitosis Hypoxia

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In vitro study of normoxic epidermal growth factor receptor-induced hypoxia-inducible factor-1-alpha, vascular endothelial growth factor, and bnip3 expression in head and neck squamous cell carcinoma cell lines: Implications for anti-epidermal growth factor receptor therapy

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HEAD AND NECK-JOURNAL FOR THE SCIENCES AND SPECIALTIES OF THE HEAD AND NECK 2015年第8期37卷 1150-1162页

作者： Secades, Pablo de Santa-Maria, Ines Saenz Merlo, Anna Suarez, Carlos Chiara, Maria-Dolores Univ Oviedo Serv Otorrinolaringol Hosp Univ Cent Asturias Inst Univ Oncol Principado Asturias Oviedo Spain

BackgroundWe previously showed that activation of epidermal growth factor receptor (EGFR) induces hypoxia inducible factor-1 (HIF-1) in head and neck squamous cell carcinoma (HNSCC) cells. In this study, we have furthered this by investigating the mechanism of HIF-1 activation by epidermal growth factor (EGF) and its association with the sensitivity to gefitinib. MethodsEGFR/HIF-1 signaling was tested by immunoblot, polymerase chain reaction (PCR), cell proliferation, and apoptosis assays. ResultsHIF-1 accumulated in cells overexpressing EGF and phosphorylated epidermal growth factor receptor (pEGFR), phosphatidylinositol-3-kinase (pPI3K), and mitogen-activated protein kinase (pMAPK). EGF-induced expression of HIF-1 and its targets, vascular endothelial growth factor (VEGF) and bnip3, were blocked by gefitinib and PI3K-inhibitors and MAPK-inhibitors. HIF-1-siRNAs abrogated EGF-induced bnip3 but not VEGF expression. Gefitinib inhibited cell proliferation and induced apoptosis more strongly in cells with constitutively active EGFR/HIF-1 signaling than in cells lacking activation of these pathways. HIF-1-siRNA treatment reduced sensitivity to gefitinib. ConclusionThe search for molecular predictors of sensitivity to gefitinib in HNSCC should be extended to the activation status of EGFR-downstream pathways, phosphorylated protein kinase B, pMAPK, and HIF-1. (c) 2014 Wiley Periodicals, Inc. Head Neck37: 1150-1162, 2015

关键词： head and neck squamous cell carcinoma epidermal growth factor hypoxia inducible factor bnip3 gefitinib

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Role of bnip3 and NIX in cell death, autophagy, and mitophagy

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CELL DEATH AND DIFFERENTIATION 2009年第7期16卷 939-946页

作者： Zhang, J. Ney, P. A. St Jude Childrens Hosp Dept Biochem Memphis TN 38117 USA Univ Tennessee Hlth Sci Ctr Integrated Program Biomed Sci Memphis TN 38126 USA

bnip3 and NIX are proteins related to the BH3-only family, which induce both cell death and autophagy. Consistent with their ability to induce cell death, bnip3 and NIX are implicated in the pathogenesis of cancer and heart disease. In tumor cells, bnip3 and NIX are regulated by hypoxia, and the deregulation of bnip3 or NIX expression is associated with tumor growth. In heart muscle, bnip3 and NIX are regulated by hypoxia and G alpha q-dependent signaling, respectively, and their expression is associated with decreased myocardial function. Apart from their role in cell death, bnip3 and NIX are also implicated in the induction of autophagy. In erythroid cells, NIX is required for a specialized type of autophagy that targets mitochondria for elimination (mitophagy). Similarly, bnip3 regulates mitophagy in response to hypoxia. In this review, we will discuss possible mechanisms by which bnip3 and NIX induce cell death and mitophagy. We will also consider the potential relationship between cell death pathways and autophagy in development and homeostasis. Cell Death and Differentiation (2009) 16, 939-946;doi: 10.1038/cdd.2009.16;published online 20 February 2009

关键词： bnip3 NIX autophagy mitophagy

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The mitophagy receptor bnip3 is critical for the regulation of metabolic homeostasis and mitochondrial function in the nucleus pulposus cells of the intervertebral disc

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AUTOPHAGY 2023年第6期19卷 1821-1843页

作者： Madhu, Vedavathi Hernandez-Meadows, Miriam Boneski, Paige K. Qiu, Yunping Guntur, Anyonya R. Kurland, Irwin J. Barve, Ruteja A. Risbud, Makarand V. Thomas Jefferson Univ Sidney Kimmel Med Coll Dept Orthopaed Surg Philadelphia PA USA Mayo Clin Dept Neurosci Jacksonville FL USA Albert Einstein Coll Med Einstein Mt Sinai Diabet Res Ctr ES DRC Bronx NY USA Maine Med Ctr Res Inst Ctr Mol Med Scarborough ME USA Washington Univ Genome Technol Access Ctr Sch Med Dept GenetMcDonnell Genome Inst St Louis MO USA Thomas Jefferson Univ Dept Orthopaed Surg 1025 Walnut StSuite 511 Coll Bldg Philadelphia PA 19107 USA

The contribution of mitochondria to the metabolic function of hypoxic NP cells has been overlooked. We have shown that NP cells contain networked mitochondria and that mitochondrial translocation of bnip3 mediates hypoxia-induced mitophagy. However, whether bnip3 also plays a role in governing mitochondrial function and metabolism in hypoxic NP cells is not known. bnip3 knockdown altered mitochondrial morphology, and number, and increased mitophagy. Interestingly, bnip3 deficiency in NP cells reduced glycolytic capacity reflected by lower production of lactate/H+ and lower ATP production rate. Widely targeted metabolic profiling and flux analysis using 1-2-C-13-glucose showed that the bnip3 loss resulted in redirection of glycolytic flux into pentose phosphate and hexosamine biosynthesis as well as pyruvate resulting in increased TCA flux. An overall reduction in one-carbon metabolism was noted suggesting reduced biosynthesis. (UC)-C-13-glutamine flux analysis showed preservation of glutamine utilization to maintain TCA intermediates. The transcriptomic analysis of the bnip3-deficient cells showed dysregulation of cellular functions including membrane and cytoskeletal integrity, ECM-growth factor signaling, and protein quality control with an overall increase in themes related to angiogenesis and innate immune response. Importantly, we observed strong thematic similarities with the transcriptome of a subset of human degenerative samples. Last, we noted increased autophagic flux, decreased disc height index and aberrant COL10A1/collagen X expression, signs of early disc degeneration in young adult bnip3 knockout mice. These results suggested that in addition to mitophagy regulation, bnip3 plays a role in maintaining mitochondrial function and metabolism, and dysregulation of mitochondrial homeostasis could promote disc degeneration.

关键词： bnip3 disc degeneration hypoxia intervertebral disc metabolism mitochondria mitophagy nucleus pulposus

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A20 ameliorates disc degeneration by suppressing mTOR/bnip3 axis-mediated mitophagy

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GENES & GENOMICS 2023年第5期45卷 657-671页

作者： Peng, Xin Zhang, Cong Gao, Jia-Wei Wang, Feng Bao, Jun-Ping Zhou, Zhi-Min Sun, Rui Ji, Hang-Yu Vlf, Cabral Wu, Xiao-Tao Med Sch Southeast Univ Nanjing Peoples R China Southeast Univ Zhongda Hosp Dept Orthoped Nanjing Peoples R China

Background The pathological mechanism of intervertebral disc degeneration (IDD) is an unanswered question that we are committed to exploring. A20 is an anti-inflammatory protein of nucleus pulposus (NP) cells and plays a protective role in intervertebral disc degeneration. Objective This study aims to investigate the molecular mechanism by which A20 attenuates disc degeneration. Methods The proteins of interest were measured by immunoblotting, immunofluorescence, ELISA assay, and immunohistochemical technique to conduct related experiments. Immunofluorescence assays and mitochondrial membrane potential (JC-1) were used to assess mitophagy and mitochondrial fitness, respectively. Results Here, we demonstrated that A20 promoted mitophagy, attenuated pyroptosis, and inhibited the degradation of the extracellular matrix, consequently significantly ameliorating disc degeneration. Mechanistically, A20 reduces pyroptosis and further suppresses cellular mTOR activity. On the one hand, A20-induced mTOR inhibition triggers bnip3-mediated mitophagy to ensure mitochondrial fitness under LPS stimulation, as a result of mitigating mitochondrial dysfunction induced by LPS. On the other hand, A20-induced mTOR inhibition reduces the loss of mitochondrial membrane potential and the generation of Mitochondrial ROS. Conclusion The study revealed that A20 promotes bnip3-mediated mitophagy by suppressing mTOR pathway activation against LPS-induced pyroptosis.

关键词： A20 Mitophagy mTOR bnip3 NLRP3

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Resistance to Hypoxia-Induced, bnip3-Mediated Cell Death Contributes to an Increase in a CD133-Positive Cell Population in Human Glioblastomas In Vitro

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JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY 2012年第12期71卷 1086-1099页

作者： Kahlert, Ulf Dietrich Maciaczyk, Donata Dai, Fangping Claus, Rainer Firat, Elke Doostkam, Soroush Bogiel, Tomasz Carro, Maria Stella Doebroessy, Mate Herold-Mende, Christel Niedermann, Gabriele Prinz, Marco Nikkhah, Guido Maciaczyk, Jaroslaw Univ Freiburg Med Ctr Dept Gen Neurosurg D-79106 Freiburg Germany Univ Freiburg Med Ctr Div Stereotact Neurosurg D-79106 Freiburg Germany Univ Heidelberg Med Ctr Dept Neurosurg Div Neurosurg Res Heidelberg Germany Univ Freiburg Fac Biol D-79106 Freiburg Germany Univ Freiburg Med Ctr Dept Neuropathol D-79106 Freiburg Germany Univ Freiburg BIOSS Ctr Biol Signaling Studies D-79106 Freiburg Germany 10th Mil Clin Hosp Dept Pathomorphol Clin Genet Lab Bydgoszcz Poland Univ Med Ctr Freiburg Dept Med 1 Div Hematol Oncol Freiburg Germany

In addition to intrinsic regulatory mechanisms, brain tumor stemlike cells (BTSCs), a small subpopulation of malignant glial tumor-derived cells, are influenced by environmental factors. Previous reports showed that lowering oxygen tension induced an increase of BTSCs expressing CD133 and other stem cell-related genes and more pronounced clonogenic capacity in vitro. We investigated the mechanisms responsible for hypoxia-dependent induction of CD133-positive BTSCs in glioblastomas. We confirmed that cultures exposed to lowered oxygen levels showed a severalfold increase of CD133-positive BTSCs. Both the increase of CD133-positive cells and deceleration of the growth kinetics were reversible after transfer to normoxic conditions. Exposure to hypoxia induced bnip3 (BCL2/adenovirus E1B 19-kDa protein-interacting protein 3)-dependent apoptosis preferentially in CD133-negative cells. In contrast, CD133-positive cells proved to be more resistant to hypoxia-induced programmed cell death. Application of the demethylating agent 5'-azacitidine resulted in an increase of bnip3 expression levels in CD133-positive cells. Thus, epigenetic modifications led to their better survival in lowered oxygen tension. Moreover, the, hypoxia-induced increase of CD133-positive cells was inhibited after 5'-azacitidine treatment. These results suggest the possible efficacy of a novel therapy for glioblastoma focused on eradication of BTSCs by modifications of epigenetic regulation of gene expression.

关键词： Apoptosis bnip3 Brain tumor stemlike cells CD133 Glioblastoma Hypoxia Promoter methylation

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Yessotoxin induces ER-stress followed by autophagic cell death in glioma cells mediated by mTOR and bnip3

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CELLULAR SIGNALLING 2014年第2期26卷 419-432页

作者： Rubiolo, J. A. Lopez-Alonso, H. Martinez, P. Milian, A. Cagide, E. Vieytes, M. R. Vega, F. V. Botana, L. M. USC Fac Vet Dept Farmacol Lugo 27002 Spain Univ Santiago Compostela Fac Vet Dept Genet Lugo 27002 Spain Lab CIFGA SA Lugo 27002 Spain Univ Santiago de Compostela Fac Vet Dept Fisiol Lugo 27002 Spain

Yessotoxin at nanomolar concentrations can induce programmed cell death in different model systems. Paraptosis-like cell death induced by YTX in BC3H1 cells, which are insensitive to several caspase inhibitors, has also been reported. This makes yessotoxin of interest in the search of molecules that target cancer cells vulnerabilities when resistance to apoptosis is observed. To better understand the effect of this molecule at the molecular level on tumor cells, we conducted a transcriptomic analysis using 3 human glioma cell lines with different sensitivities to yessotoxin. We show that the toxin induces a deregulation of the lipid metabolism in glioma cells as a consequence of induction of endoplasmic reticulum stress. The endoplasmic reticulum stress in turn arrests the cell cycle and inhibits the protein synthesis. In the three cell lines used we show that YTX induces autophagy, which is involved in cell death. The sensibility of the cell lines used towards autophagic cell death was related to their doubling time, being the cell line with the lowest proliferation rate the most resistant. The involvement of mTOR and bnip3 in the autophagy induction was also determined. (C) 2013 Elsevier Inc. All rights reserved.

关键词： Yessotoxin Autophagic cell death ER-stress bnip3 mTOR Lipid metabolism

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