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New relationship of E2F1 and bnip3 with caveolin-1 in lung cancer-associated fibroblasts

THORACIC CANCER 2020年第6期11卷 1369-1371页

作者： Shen, Cheng Chen, Xuanming Xiao, Kai Che, Guowei Sichuan Univ West China Hosp Dept Thorac Surg Chengdu 610041 Peoples R China Sichuan Univ West China Hosp Sch Med Chengdu Peoples R China Sichuan Kangcheng Biotechnol Co Ltd Chengdu Peoples R China

In recent years, studies have found that E2F1, a downstream effector of caveolin-1 (Cav-1), participates in tumor cell metabolic reprogramming. E2F1 modulates mitochondrial fusion and mitophagy. Bioinformatic analysis has identified the E2F1-MFN2 axis as a regulator of mitophagy. Our data establish a new novel paradigm for regulation of the tumor cell metabolic reprogramming pathway by Cav-1 that is operationally linked and mutually dependent on the transcriptional activation of E2F1 and induces mitophagy with bnip3 in cancer-associated fibroblasts (CAFs).

关键词： bnip3 cancer-associated fibroblasts caveolin-1 E2F1 mitophagy

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Placental localization and expression of the cell death factors bnip3 and Nix in preeclampsia, intrauterine growth retardation and HELLP syndrome

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EUROPEAN JOURNAL OF OBSTETRICS & GYNECOLOGY AND REPRODUCTIVE BIOLOGY 2005年第2期122卷 172-176页

作者： Stepan, H Leo, C Purz, S Höckel, M Horn, LC Univ Leipzig Dept Obstet & Gynecol D-04103 Leipzig Germany Univ Leipzig Inst Pathol Div Gynecol & Perinatal Pathol D-04103 Leipzig Germany

Objective: bnip3 and its homologue Nix are pro-apoptotic factors of the Bcl-2-family and are expressed in malignant tumors. In vitro, this expression was shown to be mediated by hypoxia. Recently, it has been shown that placental hypoxia as well as apoptosis are pathogenetic factors for pregnancy-induced hypertensive diseases and intrauterine growth retardation (IUGR). The aim of the study was to analyze placental expression of bnip3 and Nix in pregnancies complicated by preeclampsia, hemolysis, elevated liver enzymes and low platelets (HELLP) syndrome and IUGR. Material and methods: Placental tissue was sampled from 10 pregnancies each with preeclampsia, HELLP syndrome, IUGR and gestational age-matched controls. The placental expression of bnip3/Nix has been investigated with immunohistochemistry by the use of specific human bnip3/Nix antibodies. Results: In cytotrophoblastic cells, the bnip3 expression was strong in the control placentas, but only mediate in the placentas from pregnancies with preeclampsia, IUGR or HELLP syndrome. The intensity of the Nix staining showed a similar pattern. In the syncytiotrophoblast, there was a weak bnip3 staining observable in the control as well as IUGR samples, whereas bnip3 was undetectable in preeclamptic placentas or those with HELLP syndrome. For Nix, only in the preeclampsia a weak staining was detectable, whereas all other probes were negative. Conclusions: Our study shows for the first time that the pro-apoptotic proteins bnip3 and Nix are expressed in the human placenta. Pregnancies with placental dysfunction and hypertensive pregnancy disorders with different clinical manifestations are characterized by a significantly decreased expression of bnip3 and Nix. These results suggest that the hypothesis of generally increased placental apoptosis in pregnancy-induced hypertensive disorders caused by disturbed trophoblast invasion has to be partly reconsidered. (c) 2005 Elsevier Ireland Ltd. All rights reserved.

关键词： apoptosis preeclampsia bnip3 HELLP syndrome intrauterine growth retardation

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Regulation of bnip3 in normal and cancer cells

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MOLECULES AND CELLS 2006年第1期21卷 1-6页

作者： Lee, H Paik, SG Chungnam Natl Univ Sch Biosci & Biotechnol Dept Biol Taejon 305764 South Korea Chungnam Natl Univ Inst Biotechnol Taejon 305764 South Korea

Bcl-2/adenovirus E1B 19 kDa-interacting protein 3 (bnip3) is a mitochondrial pro-apoptotic protein that has a single Bcl-2 homology 3 (BH3) domain and a COOH-terminal transmembrane (TM) domain. Although it belongs to the Bcl-2 family and can hetero-dimerize with Bcl-2, its pro-apoptotic activity is distinct from those of other members of the Bcl-2 family. For example, cell death mediated by bnip3 is independent of caspases and shows several characteristics of necrosis. Furthermore, the TM domain, but not the BH3 domain, is required for dimerization, mitochondrial targeting and pro-apoptotic activity. bnip3 plays an important role in hypoxia-induced death of normal and malignant cells. Its expression is markedly increased in the hypoxic regions of some solid tumors and appears to be regulated by hypoxia-inducible factor (HIF), which binds to a site on the bnip3 promoter. Silencing, followed by methylation, of the bnip3 gene occurs in a significant proportion of cancer cases, especially in pancreatic cancers. bnip3 also has a role in the death of cardiac myocytes in ischemia. Further studies of bnip3 should provide insight into hypoxic cell death and may contribute to improved treatment of cancers and cardiovascular diseases.

关键词： apoptosis Bcl-2 BH3 bnip3 hypoxia

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Epigenetic Regulation of E2F-1-Dependent bnip3 Transcription and Cell Death by Nuclear Factor-κB and Histone Deacetylase-1

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PEDIATRIC CARDIOLOGY 2011年第3期32卷 263-266页

作者： Gang, Hongying Dhingra, Rimpy Wang, Yan Mughal, Wajihah Gordon, Joseph W. Kirshenbaum, Lorrie A. St Boniface Gen Hosp Res Ctr Dept Pharmacol & Therapeut Fac MedInst Cardiovasc Sci Winnipeg MB R2H 2A6 Canada St Boniface Gen Hosp Res Ctr Dept Physiol Fac MedInst Cardiovasc Sci Winnipeg MB R2H 2A6 Canada

A delicate balance exists between cell growth and cell death. In the context of the adult myocardium, inappropriate or inordinate cell loss through an apoptotic process may profoundly influence cardiac structure, function, or both given the limited and meager ability of the heart for repair after injury. Earlier work by the authors' laboratory identified a close relation between cell cycle factor E2F-1 and hypoxia-inducible factor bnip3 as the key regulator of apoptosis and autophagy in ventricular myocytes. Epigenetic changes by histone-modifying proteins, namely, histone deacetylases (HDACs) influence cell survival by altering the activity of histone core proteins, transcription factors, or both. This report highlights the intricate nature between the cellular factors E2F-1 and nuclear factor-kappa B (NF-kappa B) and the epigenetic regulation of bnip3 gene transcription by HDAC1 for cell survival of ventricular myocytes.

关键词： Apoptosis bnip3 E2F-1 Histone deacetylases Mitochondrion NF-kappa B

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An unexpected journey for bnip3

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AUTOPHAGY 2024年第6期20卷 1447-1448页

作者： Delgado, Jose M. Shoemaker, Christopher J. Dartmouth Coll Geisel Sch Med Dept Biochem & Cell Biol Hanover NH USA Dartmouth Canc Ctr Lebanon NH USA Dartmouth Coll Geisel Sch Med Dept Biochem & Cell Biol Hanover NH 03755 USA

Mitophagy is a cellular process that enables the selective degradation of damaged, dysfunctional, or superfluous mitochondria. During mitophagy, specific proteins recognize and tag mitochondria for degradation. These tagged mitochondria are engulfed by specialized structures called phagophores that then mature into autophagosomes/mitophagosomes. Mitophagosomes subsequently transport their mitochondrial cargo to lysosomes, where the mitochondria are broken down and recycled. While the PINK1-PRKN-dependent mitophagy pathway is well understood, mitophagy can also occur independently of this pathway. bnip3 and bnip3L/NIX, paralogous membrane proteins on the outer mitochondrial membrane (OMM), serve as ubiquitin-independent mitophagy receptors. Historically, bnip3 regulation was thought to be primarily transcriptional through HIF1A (hypoxia inducible factor 1 subunit alpha). However, recent work has revealed a significant post-translational dimension, highlighting the strong role of the ubiquitin-proteasome system (UPS) in bnip3 regulation. With these emerging concepts in mind, we aimed to develop a unified understanding of how steady-state levels of bnip3 are established and maintained and how this regulation governs underlying cell physiology.

关键词： bnip3 ER membrane protein complex EMC membrane trafficking mitophagy NIX

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Regulation of mitochondrial integrity, autophagy and cell survival by bnip3

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AUTOPHAGY 2007年第6期3卷 616-619页

作者： Tracy, Kristin Macleod, K. F. Univ Chicago Ben May Dept Canc Res Chicago IL 60637 USA

Understanding the role of bnip3 in the systemic response to hypoxia has been complicated by conflicting results that indicate on the one hand that bnip3 promotes cell death, and other data, including our own that bnip3 is not sufficient for cell death, but rather plays a critical role in hypoxia-induced autophagy. This work suggests that rather than promoting death, bnip3 may actually allow survival either by preventing ATP depletion or by eliminating damaged mitochondria. However, the function of bnip3 may be subverted under unusual conditions associated with acidosis that arise following extended periods of hypoxia and anaerobic glycolysis. Despite this novel insight into bnip3 function, much remains to be done in terms of pinning down a molecular activity for bnip3 that explains both its role in autophagy and how this may be subverted to induce cell death. As a target of the RB tumor suppressor, our work also places bnip3 at the center of efforts to exploit autophagy to better treat human cancers in which tumor hypoxia is implicated as a progression factor.

关键词： bnip3 hypoxia mitochondria autophagy reactive oxygen species necrosis cancer

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Post-Translational Control of bnip3 and Mitophagy by ULK1 Kinase

Post-Translational Control of BNIP3 and Mitophagy by ULK1 Ki...

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作者： Poole, Logan Patrick The University of Chicago

学位级别：Ph.D., Doctor of Philosophy

bnip3 is a mitochondrial cargo receptor that specifically targets mitochondria for degradation at the autolysosome through a specialized form of autophagy called mitophagy. bnip3 is transcriptionally upregulated in response to a number of stressors, including hypoxia, where it functions to decrease mitochondrial mass, limit ROS, and promote the efficient use of limiting metabolites and oxygen. ULK1, the catalytic component of the autophagy initiation complex, is best known for its role in stimulating general autophagy, however recent work has demonstrated that ULK1 may also promote mitophagy. The mechanism through which ULK1 specifically promotes mitophagy remains poorly understood. Here we show that ULK1 phosphorylates bnip3 on a critical serine residue (S17) adjacent to its amino terminal LIR motif to promote its interaction with LC3 and mitophagy. Similarly, we found that ULK1 phosphorylates the bnip3 homolog, bnip3L, on a homologous serine residue (S35), suggestive of an expanded role of ULK1 in the specific regulation of mitophagy. Additionally, we determined that ULK1 interaction promotes the stability of bnip3 protein by limiting its turnover at the proteasome independent of S17 phosphorylation. This stabilization of bnip3 protein by ULK1 requires an intact bnip3 “BH3” domain, and deletion of this domain increases bnip3 protein levels and decreases bnip3 turnover independent of ULK1. We found that this process of bnip3 protein stabilization was critical to the increase in bnip3 protein levels upon hypoxic stress, as inhibition of ULK1 blocked bnip3 protein upregulation in response to hypoxia. Together, the work in this thesis expands our understanding of the mechanism through which ULK1 specifically regulates mitophagy through the stabilization and phosphorylation of bnip3.

关键词： Autophagy bnip3 Mitophagy ULK1

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Isolation of Rab5-positive endosomes reveals a new mitochondrial degradation pathway utilized by bnip3 and Parkin

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Small GTPases 2020年第1期11卷 69-76页

作者： Hammerling, Babette C. Shires, Sarah E. Leon, Leonardo J. Cortez, Melissa Q. Gustafsson, Åsa B. Skaggs School of Pharmacy and Pharmaceutical Sciences University of California San Diego La Jolla CA United States

Degradation of mitochondria is an important cellular quality control mechanism mediated by two distinct pathways: one involving Parkin-mediated ubiquitination and the other dependent on mitophagy receptors. It is known that mitochondria are degraded by the autophagy pathway;however, we recently reported that the small GTPase Rab5 and early endosomes also participate in Parkin-mediated mitochondrial clearance. Here, we have developed a protocol to isolate Rab5-positive vesicles from cells for proteomics analysis and provide additional data confirming that mitophagy regulators and mitochondrial proteins are present in these vesicles. We also demonstrate that the mitophagy receptor bnip3 utilizes the Rab5-endosomal pathway to clear mitochondria in cells. These findings indicate that a redundancy exists in the downstream degradation pathways to ensure efficient mitochondrial clearance. © 2017, © 2017 Taylor & Francis.

关键词： autophagy bnip3 endosomes mitochondria mitophagy Parkin Rab5

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bnip3 Regulates at101 [(-)-Gossypol] Induced Death in Malignant Peripheral Nerve Sheath Tumor Cells

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2016年

作者： niroop kaza

bnip3 Regulates at101 [(-)-Gossypol] Induced Death in Malignant Peripheral Nerve Sheath Tumor Cells. by Kaza, Niroop; Kohli, Latika; Graham, Christopher D.; Klocke, Barbara J.; Carroll, Steven L.; Roth, Kevin A.; publ... 详细信息

关键词： [(-)-gossypol] at101 bnip3 cells. death

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bnip3 is essential for mediating 6-thioguanine-and 5-fluorouracil-induced autophagy following DNA mismatch repair processing

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细胞研究（英文版） 2010年第6期20卷 665-675页

作者： Xuehuo Zeng Timothy J Kinsella Department of Radiation Oncology The Case Integrative Cancer Biology Program Case Western Reserve University ClevelandOH44106 USA

DNA mismatch repair (MMR) processes the chemically induced mispairs following treatment with clinically important nucleoside analogs such as 6-thioguanine (6-TG) and 5-fluorouracil (5-FU). MMR processing of these drugs has been implicated in activation of a prolonged G2/M cell cycle arrest for repair and later induction of apoptosis and/or autophagy for irreparable DNA damage. In this study, we investigated the role of Bcl2 and adenovirus E1B Nineteen-kilodalton Interacting Protein (bnip3) in the activation of autophagy, and the temporal relationship between a G2/M cell cycle arrest and the activation of bnip3-mediated autophagy following MMR processing of 6-TG and 5-FU. We found that bnip3 protein levels are upregulated in a MLH1 (MMR+)-dependent manner following 6-TG and 5-FU treatment. Subsequent small-interfering RNA (siRNA)-mediated bnip3 knockdown abrogates 6-TG-induced autophagy. We also found that p53 knockdown or inhibition of mTOR activity by rapamycin cotreatment impairs 6-TG- and 5-FU-induced upregulation of bnip3 protein levels and autophagy. Furthermore, suppression of Checkpoint kinase 1 (Chk1) expression with a subsequent reduction in 6-TG-induced G2/M cell cycle arrest by Chk1 siRNA promotes the extent of 6-TG-induced autophagy. These findings suggest that bnip3 mediates 6-TG- and 5-FU-induced autophagy in a p53- and mTOR-dependent manner. Additionally, the duration of Chk1-activated G2/M cell cycle arrest determines the level of autophagy following MMR processing of these nucleoside analogs.

关键词： bnip3 p53 mTOR autophagy nucleoside analogs

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