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作者：于大堂第三军医大学

学位级别：硕士

目的研究大鼠脊髓损伤后脊髓组织神经元自噬与线粒体自噬的表达变化以及线粒体自噬相关蛋白bnip3、NIX和p53在大鼠脊髓损伤后不同时间点的表达变化及意义，探讨新的脊髓损伤继发性神经元死亡发生机制。方法健康雄性SD大鼠，体重200-220... 详细信息

目的研究大鼠脊髓损伤后脊髓组织神经元自噬与线粒体自噬的表达变化以及线粒体自噬相关蛋白bnip3、NIX和p53在大鼠脊髓损伤后不同时间点的表达变化及意义，探讨新的脊髓损伤继发性神经元死亡发生机制。方法健康雄性SD大鼠，体重200-220g，取16只随机分为假手术组(n=8)和脊髓损伤后24h组(n=8)，用于透射电镜和免疫荧光检测。另取48只随机分为假手术组，损伤后6h、24h、48h、72h、96h组(n=8)，用于荧光定量PCR(real-time PCR)和Westernblot检测。Allen’s法建立脊髓损伤模型，假手术组仅作T10椎板切除。各组在术前及术后6h、24h、48h、72h、96h采用BBB评分法评价大鼠后肢运动功能变化情况；透射电镜观测损伤组织的超微结构；荧光定量PCR检测bnip3mRNA的表达变化；Western blot检测LC3、bnip3、NIX、p53的表达变化；免疫荧光检测LC3Ⅱ、bnip3的表达及定位。结果 1、假手术组中神经元细胞核膜完整，胞质中粗面内质网以及线粒体等细胞器形态正常，未见自噬体及线粒体自噬体；脊髓损伤后24h观测到神经元线粒体肿胀、空泡的形成，高倍镜下检测到神经元自噬体及线粒体自噬体。 2、荧光定量PCR检测发现bnip3mRNA的表达量在损伤后6h明显升高，并在24h达到高峰(p <0.01)。 3、Western blot检测发现LC3-II/LC3I的水平24h后明显升高，96h仍有较高表达(p <0.01)；bnip3、p53的表达量在6h明显升高，并在24h达到高峰(p <0.01)，96h下降至损伤前水平；NIX的表达量在6h后明显升高(p <0.01)，96h仍有较高表达(p <0.01)。 4、免疫荧光显示LC3II、bnip3在脊髓损伤后24h神经元中高表达。结论 1.大鼠脊髓损伤后神经元自噬以及线粒体自噬被诱导激活。 2.线粒体自噬相关蛋白bnip3、NIX在脊髓损伤后表达增高并可能参与线粒体自噬的诱导。

关键词：脊髓损伤自噬线粒体自噬 LC3 bnip3 NIX p53

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Enhancing lysosome biogenesis attenuates bnip3-induced cardiomyocyte death

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AUTOPHAGY 2012年第3期8卷 297-309页

作者： Ma, Xiucui Godar, Rebecca J. Liu, Haiyan Diwan, Abhinav Washington Univ Sch Med Dept Internal Med Ctr Cardiovasc ResDiv Cardiol St Louis MO 63110 USA John Cochran VA Med Ctr St Louis MO USA

Hypoxia-inducible pro-death protein bnip3 (BCL-2/adenovirus E1B 19-kDa interacting protein 3), provokes mitochondrial permeabilization causing cardiomyocyte death in ischemia-reperfusion injury. Inhibition of autophagy accelerates bnip3-induced cell death, by preventing removal of damaged mitochondria. We tested the hypothesis that stimulating autophagy will attenuate bnip3-induced cardiomyocyte death. Neonatal rat cardiac myocytes (NRCMs) were adenovirally transduced with bnip3 (or LacZ as control;at multiplicity of infection = 100);and autophagy was stimulated with rapamycin (100 nM). Cell death was assessed at 48 h. bnip3 expression increased autophagosome abundance 8-fold and caused a 3.6-fold increase in cardiomyocyte death as compared with control. Rapamycin treatment of bnip3-expressing cells led to further increase in autophagosome number without affecting cell death. bnip3 expression led to accumulation of autophagosome-bound LC3-II and p62, and an increase in autophagosomes, but not autolysosomes (assessed with dual fluorescent mCherry-GFP-LC3 expression). bnip3, but not the transmembrane deletion variant, interacted with LC3 and colocalized with mitochondria and lysosomes. However, bnip3 did not target to lysosomes by subcellular fractionation, provoke lysosome permeabilization or alter lysosome pH. Rather, bnip3-induced autophagy caused a decline in lysosome numbers with decreased expression of the lysosomal protein LAMP-1, indicating lysosome consumption and consequent autophagosome accumulation. Forced expression of transcription factor EB (TFEB) in bnip3-expressing cells increased lysosome numbers, decreased autophagosomes and increased autolysosomes, prevented p62 accumulation, removed depolarized mitochondria and attenuated bnip3-induced death. We conclude that bnip3 expression induced autophagosome accumulation with lysosome consumption in cardiomyocytes. Forced expression of TFEB, a lysosomal biogenesis factor, restored autophagosome processing an

关键词： bnip3 autophagy cardiomyocyte death lysosomes TFEB

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低氧环境下的线粒体自噬受体的进化与脊椎动物从水生到陆地的演化一致

低氧环境下的线粒体自噬受体的进化与脊椎动物从水生到陆地的演化...

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浙江省生物信息学学会第五届学术年会暨大数据时代精准医学国际学术研讨会

作者：吴晓梅吴飞华邬倩荣张庶陈素萍 Matthew Sima College of Life and Environmental Sciences Hangzhou Normal University Department of Biology Duke University College of life sciences Zhejiang University

由于动物进化出了利用氧气和线粒体的氧化磷酸化过程合成ATP,适应多变的氧气浓度的能力是进化压力的一个重要组成部分。目前已知三个线粒体自噬受体(FUNDC1,bnip3 and NIX),在哺乳动物细胞长期处于低氧环境下,这三个受体蛋白引导下游通... 详细信息

由于动物进化出了利用氧气和线粒体的氧化磷酸化过程合成ATP,适应多变的氧气浓度的能力是进化压力的一个重要组成部分。目前已知三个线粒体自噬受体(FUNDC1,bnip3 and NIX),在哺乳动物细胞长期处于低氧环境下,这三个受体蛋白引导下游通路,清理掉功能失调的线粒体(即线粒体自噬),从而维持氧气的动态平衡和阻止细胞死亡。然而,人们对这些受体的进化起源以及结构与功能之间的关系还知之甚少。首先,我们发现含FUN14结构域的蛋白质分布于古细菌、细菌和真核基因组,不过含bnip3结构域的蛋白质起源于早期动物。然后,我们分析这些人类线粒体自噬受体的关键氨基酸残基的保守性。这些关键残基主要通过磷酸化参与受体调节和与LC3相互作用。FUNDC1可能在脊椎动物的早期进化中获得了通过后翻译调控绑定LC3的能力,而bnip3和NIX与LC3互作的能力可以追溯到早期无脊椎动物。有意思的是,FUNDC1和bnip3在鱼类中都缺失了一层磷酸化调控,这些调控在陆地脊椎动物中却是保守的。分子进化分析揭示了bnip3、NIX(两者的表达量受到感知氧气浓度的HIF-1α的直接调控)和HIF-1α在鱼类中具有比哺乳动物更高的替换率;相反地,FUNDC1和其上游的调控蛋白之一MARCH5在哺乳动物中显示更高的替换率。因此,我们提出假设:线粒体自噬受体的结构在陆地脊椎动物和鱼类中的进化痕迹可能反映了脊椎动物从水生到陆地演化的过程;在这个过程中,大气中的氧气浓度扮演了脊椎动物进化历程的一种选择驱动力。总之,我们的工作结合以前的实验结果显示FUDNC1/MARCH5所调控的低氧诱导的线粒体自噬和bnip3/NIX所调控的依赖于HIF-1α的线粒体自噬或许采用了不同的分子机制。

关键词：线粒体自噬低氧氧气浓度 FUNDC1 bnip3 NIX 分子进化陆地脊椎动物

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Bcl-2/adenovirus E1B 19 kDa-interacting protein 3 (bnip3) expression is epigenetically regulated by one-carbon metabolism in invasive duct cell carcinoma of breast

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MOLECULAR AND CELLULAR BIOCHEMISTRY 2012年第1-2期361卷 189-195页

作者： Naushad, Shaik Mohammad Prayaga, Aruna Digumarti, Raghunadha Rao Gottumukkala, Suryanarayana Raju Kutala, Vijay Kumar Nizams Inst Med Sci Dept Clin Pharmacol & Therapeut Hyderabad 500082 Andhra Pradesh India Nizams Inst Med Sci Dept Pathol Hyderabad 500082 Andhra Pradesh India Nizams Inst Med Sci Dept Med Oncol Hyderabad 500082 Andhra Pradesh India Nizams Inst Med Sci Dept Surg Oncol Hyderabad 500082 Andhra Pradesh India

In view of recent studies highlighting the prognostic relevance of expression and CpG island methylator phenotype (CIMP) of Bcl-2/adenovirus E1B 19 kDa-interacting protein 3 (bnip3) in invasive duct cell carcinoma (IDC), we hypothesized in this article that impaired one-carbon metabolism might influence CIMP phenotype of bnip3. In order to substantiate the prognostic relevance of bnip3, we explored its association with 8-oxo-2'deoxyguanosine (8-oxodG), a marker of oxidative stress with prognostic relevance. bnip3 expression and CIMP phenotype were studied using semi-quantitative RT-PCR and combined bisulfite restriction analysis (COBRA), respectively, in 56 IDC tumors. Eight polymorphisms in one-carbon metabolism were studied using PCR-RFLP and PCR-AFLP approaches. 8-oxodG was measured using competitive ELISA kit. bnip3 was found to be upregulated in IDC (cases vs. controls: 0.94 +/- A 0.05 vs. 0.18 +/- A 0.08, P < 0.0001). COBRA analysis confirmed hypomethylation of bnip3 promoter CpG island in these cases. CIMP phenotype of bnip3 showed positive association with tubule formation (P = 0.034) and methionine synthase reductase (MTRR) A66G (P = 0.002);inverse association with cytosolic serine hydroxyl methyltransferase (cSHMT) C1420T (P < 0.005) and 8-oxodG (< 10% vs. > 10% methylation: 7.24 +/- A 2.77 ng/ml vs. 4.42 +/- A 2.93 ng/ml, P < 0.0005);and no association with nuclear pleomorphism or mitotic index or ER, PR, and HER statuses. Synergistic effect of MTR A2756G and MTRR A66G variants on bnip3 hypermethylator phenotype was clearly evident (P < 0.0007). MTRR A66G and cSHMT C1420T polymorphisms influence CIMP phenotype of bnip3, thus epigenetically regulating bnip3 in breast cancer. The linear association between bnip3 and 8-oxodG substantiates the role of bnip3 as redox sensor as well as prognostic marker in breast cancer.

关键词： bnip3 One-carbon metabolism CpG island methylator phenotype 8-Oxo-2 '-deoxyguanosine

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Expression TGM2 and bnip3 have prognostic significance in laryngeal cancer patients receiving surgery and postoperative radiotherapy: A retrospective study

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JOURNAL OF TRANSLATIONAL MEDICINE 2012年第1期10卷 1-9页

作者： Jin, Ting Lin, Huan-Xin Lin, Hui Guo, Li-Bing Ge, Nan Cai, Xiu-Yu Sun, Rui Chen, Wen-Kuan Li, Qiu-Li Hu, Wei-Han Sun Yat Sen Univ State Key Lab Oncol S China Ctr Canc Guangzhou 510060 Guangdong Peoples R China Zhejiang Canc Hosp Dept Radiat Oncol Hangzhou 310022 Zhejiang Peoples R China Sun Yat Sen Univ Dept Radiat Oncol Ctr Canc Guangzhou 510060 Guangdong Peoples R China Guangdong Second Prov Peoples Hosp Dept Oncol Guangzhou 510060 Guangdong Peoples R China Sun Yat Sen Univ Dept Head & Neck Surg Ctr Canc Guangzhou 510060 Guangdong Peoples R China

Background: This study was designed to determine the pattern and correlation between expression of the HIF-1 alpha transcriptional targets TGM2 and bnip3 in laryngeal cancer, and investigate the association of bnip3 and TGM2 with clinical outcome in laryngeal squamous cell carcinoma (SCC) patients receiving postoperative radiotherapy. Methods: Immunostaining with antibodies specific to bnip3 and TGM2 was performed in formalin-fixed, paraffin-embedded specimens from 148 laryngeal SCC patients. bnip3 and TGM2 expression was scored as high or low, based on the number of tumor cells stained and the staining intensity. All patients received postoperative radiotherapy. Patient follow up and clinicopathological data were compared using the Chi-squared test, univariate and multivariate analyses, and survival curves were generated using the Kaplan-Meier method and log-rank test. Results: The 3, 5 and 10-year overall survival rates (OS) for all patients were 77.7%, 71.6%, 56.4%, respectively. Primary tumor site, T stage, overall stage, lymph-node metastasis, bnip3 expression and TGM2 expression were significant prognostic factors for OS in univariate analysis. Negative cervical lymph nodes, high bnip3 expression and low TGM2 expression were independent prognostic factors of improved OS in multivariate analysis. bnip3 expression correlates with TGM2 expression in laryngeal SCC (P = 0.012). Conclusions: This study indicates that lymph-node metastasis, bnip3 expression and TGM2 expression are independent prognostic factors in laryngeal SCC patients receiving postoperative radiotherapy. Further studies are required to investigate how bnip3 and/or TGM2 influence the prognosis of laryngeal SCC patients treated with postoperative radiotherapy, and to determine how TGM2 and bnip3 expression are regulated.

关键词： TGM2 bnip3 Postoperative radiotherapy Laryngeal cancer Prognosis

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线粒体自噬与心肌保护

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生理科学进展 2016年第3期47卷 215-218页

作者：王建礼刘秀华中国人民解放军总医院病理生理研究室北京100853 济宁医学院病理生理学教研室济宁272067

线粒体自噬是指细胞通过自噬的机制选择性地清除线粒体的过程。通过该途径,细胞可降解并清除受损或功能障碍的线粒体,以维持细胞内线粒体质量和数量的平衡,从而维持细胞稳态。在生理状态及应激状态下,多种因子可调控心肌细胞线粒体自噬... 详细信息

线粒体自噬是指细胞通过自噬的机制选择性地清除线粒体的过程。通过该途径,细胞可降解并清除受损或功能障碍的线粒体,以维持细胞内线粒体质量和数量的平衡,从而维持细胞稳态。在生理状态及应激状态下,多种因子可调控心肌细胞线粒体自噬,进而发挥保护心肌细胞的作用。本文就线粒体自噬及其调控机制以及其在心肌保护中的作用做一综述。

关键词：线粒体自噬 PINK1 Parkin NIX bnip3 心肌保护

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Combined effects of EGFR tyrosine kinase inhibitors and vATPase inhibitors in NSCLC cells

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TOXICOLOGY AND APPLIED PHARMACOLOGY 2015年第1期287卷 17-25页

作者： Jin, Hyeon-Ok Hong, Sung-Eun Kim, Chang Soon Park, Jin-Ah Kim, Jin-Hee Kim, Ji-Young Kim, Bora Chang, Yoon Hwan Hong, Seok-Il Hong, Young Jun Park, In-Chul Lee, Jin Kyung Korea Inst Radiol & Med Sci KIRAMS Radiat Biobank Seoul 139706 South Korea Korea Inst Radiol & Med Sci Div Radiat Canc Res Seoul 139706 South Korea Konkuk Univ Dept Microbiol Engn Seoul 143701 South Korea Korea Inst Radiol & Med Sci Dept Lab Med Korea Canc Ctr Hosp Seoul 139706 South Korea

Despite excellent initial clinical responses of non-small cell lung cancer (NSCLC) patients to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), many patients eventually develop resistance. According to a recent report, vacuolar H + ATPase (vATPase) is overexpressed and is associated with chemotherapy drug resistance in NSCLC. We investigated the combined effects of EGFR TKIs and vATPase inhibitors and their underlying mechanisms in the regulation of NSCLC cell death. We found that combined treatment with EGFR TKIs (erlotinib, gefitinib, or lapatinib) and vATPase inhibitors (bafilomycin A1 or concanamycin A) enhanced synergistic cell death compared to treatments with each drug alone. Treatment with bafilomycin A1 or concanamycin A led to the induction of bnip3 expression in an Hif-1 alpha dependent manner. Knock-down of Hif-1 alpha or bnip3 by siRNA further enhanced cell death induced by bafilomycin A1, suggesting that Hif-1 alpha/bnip3 induction promoted resistance to cell death induced by the vATPase inhibitors. EGFR TKIs suppressed Hif-1 alpha and bnip3 expression induced by the vATPase inhibitors, suggesting that they enhanced the sensitivity of the cells to these inhibitors by decreasing Hif-1 alpha/bnip3 expression. Taken together, we conclude that EGFR TKIs enhance the sensitivity of NSCLC cells to vATPase inhibitors by decreasing Hif-1 alpha/bnip3 expression. We suggest that combined treatment with EGFR TKIs and vATPase inhibitors is potentially effective for the treatment of NSCLC. (C) 2015 Elsevier Inc All rights reserved.

关键词： bnip3 Epidermal growth factor receptor Hif-1 alpha Tyrosine kinase inhibitors vATPase inhibitors

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Mending a broken heart: the role of mitophagy in cardioprotection

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AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY 2015年第3期308卷 H183-H192页

作者： Moyzis, Alexandra G. Sadoshima, Junichi Gustafsson, Asa B. Univ Calif San Diego Skaggs Sch Pharm & Pharmaceut Sci La Jolla CA 92093 USA Rutgers State Univ New Jersey Med Sch Inst Cardiovasc Res Dept Cell Biol & Mol Med Newark NJ 07102 USA

The heart is highly energy dependent with most of its energy provided by mitochondrial oxidative phosphorylation. Mitochondria also play a role in many other essential cellular processes including metabolite synthesis and calcium storage. Therefore, maintaining a functional population of mitochondria is critical for cardiac function. Efficient degradation and replacement of dysfunctional mitochondria ensures cell survival, particularly in terminally differentiated cells such as cardiac myocytes. Mitochondria are eliminated via mitochondrial autophagy or mitophagy. In the heart, mitophagy is an essential housekeeping process and required for cardiac homeostasis. Reduced autophagy and accumulation of impaired mitochondria have been linked to progression of heart failure and aging. In this review, we discuss the pathways that regulate mitophagy in cells and highlight the cardioprotective role of mitophagy in response to stress and aging. We also discuss the therapeutic potential of targeting mitophagy and directions for future investigation.

关键词： autophagy mitophagy mitochondria parkin bnip3 FUNDC1

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SIRT1通过线粒体自噬阻断NLRP3炎症小体活化和足细胞损伤

SIRT1通过线粒体自噬阻断NLRP3炎症小体活化和足细胞损伤

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作者：白咪南京医科大学

学位级别：博士

足细胞(podocyte)是一种高度分化的终末期细胞,位于肾小球毛细血管膜外,呈星形多突状,是肾小球滤过屏障的重要组成部分。足细胞损伤是肾小球硬化的关键因素,越来越多的证据表明,在多种肾小球疾病中,如膜性肾病(membranous nephropathy,... 详细信息

足细胞(podocyte)是一种高度分化的终末期细胞,位于肾小球毛细血管膜外,呈星形多突状,是肾小球滤过屏障的重要组成部分。足细胞损伤是肾小球硬化的关键因素,越来越多的证据表明,在多种肾小球疾病中,如膜性肾病(membranous nephropathy,MN)、微小病变性肾病(minimal change disease, MCD)、局灶节段肾小球硬化(focal segmental glomerulonephritis,FSGS)及糖尿病肾病(diabetic nephropathy,DN)等,足细胞损伤引起蛋白尿,加速肾小球疾病进展为肾小球硬化,最终成为慢性肾脏病(chronic kidney disease,CKD),不可避免的走向肾脏替代治疗的道路。因此,充分了解足细胞损伤发生的机制,找到控制足细胞损伤的方法,是阻断CKD发生发展的关键。炎症小体(inflammasome)由Tschopp于2002年首先提出,是指含有NOD样受体(NOD-like receptor,NLR)家族成员蛋白形成的复合体,包括NLRP1、 AIM2、NLRP3、NLRC4等炎症小体。在这些炎症小体中,对NLRP3(NOD-like receptor family,pyrin domain containing 3)炎症小体研究最多,其基本结构单位是由NLRP3、接头蛋白ASC(apoptosis speck protein with CARD)和胱天蛋白酶(cysteinyl aspartate-specific protease,caspase-)-1组成。在静息状态下无活性,当细胞受到特定刺激后,NLRP3与ASC结合,招募pro-caspase-1形成复合体,使其成为有生物活性的caspase-1,即白细胞介素(interleukin,IL) -1β转化酶,后者作用于炎症因子前体如pro-IL-18等,产生具有致炎活性的IL-18,参与机体天然免疫应答及细胞损伤。有报道表明,NLRP3炎症小体与多种肾脏疾病,如肾脏纤维化等相关。但其在足细胞损伤中的作用尚有待进一步阐明。线粒体自噬(mitophagy)在肾损伤中的作用也引起大家的关注。线粒体是能量代谢的重要场所,参与多种细胞生命活动,决定着细胞的生死。其易受到外界因素的损伤,即发生线粒体功能障碍。不需要的或受损的线粒体须被有效清除,以保证细胞进行正常的生命活动。选择性清除不需要的或者受损线粒体的过程称为线粒体自噬。自噬的异常与神经退行性疾病、糖尿病和肿瘤的发生有密切关系。有文献报道,在巨噬细胞中线粒体自噬可以抑制NLRP3炎症小体的产生,但在肾脏中尚未见报道。沉默信息调节因子2(silent information regulator 2, Sir2)一相关酶类(Sir2-related enzymes, sirtuins)是近年来发现的烟酰胺腺嘌呤二核苷酸(nicotinamide adenine dinucleotide, NAD+)依赖的第1II类组蛋白去乙酰化酶类,其中SIRT1研究最为深入。在哺乳动物中,SIRT1主要定位在细胞核,通过乙酰化活性发挥作用。在肾脏中,已有的文献报道SIRT1具有保护作用,如调节血糖和血脂代谢、保护肾小球滤过屏障、调节线粒体功能及能量代谢以及抗纤维化等。同时,SIRT1可以通过对叉头状转录因子O (forkhead box-containing protein O subfamily, FOXO)的去乙酰化调节作用,从而调控自噬的发生,在多种疾病,如糖尿病、肿瘤、肥胖、心血管等疾病中发挥重要作用。我们前期研究也发现SIRT1/PGC-la通过保护线粒体功能抑制醛固酮(Aldosterone,Aldo)诱导的足细胞损伤。综上,本研究推测,SIRT1可以通过促进线粒体自噬,阻断Aldo诱导的线粒体功能障碍,进而抑制JLRP3炎症小体,减轻足细胞损伤,发挥保护作用。为探讨其中的机制,我们进行了如下研究,实验分为三部分。第一部分NLRP3炎症小体在醛固酮诱导的足细胞损伤中的作用目的：探讨NLRP3炎症小体活化在Aldo诱导的足细胞损伤中的作用。方法：免疫组织化学染色检测慢性肾脏病(MCD、FSGS)患儿肾组织中NLRP3的表达。体外培养小鼠足细胞系MPC5,应用不同浓度的Aldo (25、50、100、 200 nM)刺激不同的时间(2、4、8、12、24、48 h)。体外应用NLRP3 siRNA转染足细胞24h,加Aldo刺激,分为四组：阴性对照组(negative control,NC)、 NC+Aldo组、NLRP3 siRNA组、NLRP3 siRNA+Aldo组。体外应用MnTBAP、CsA预处理足细胞30min,再加用Aldo刺激,分组如

关键词：足细胞线粒体功能障碍 NLRP3炎症小体 Aldo SIRT1 线粒体功能障碍 NLRP3炎症小体 Aldo 足细胞 bnip3 线粒体自噬 SIRT1 线粒体功能障碍 NLRP3 Aldo 足细胞

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bnip3在肾透明细胞癌中的表达及其与HIF-1α、VEGF的相关性研究

引用

四川大学学报（医学版） 2012年第1期43卷 79-82页

作者：罗琳熊子兵曾浩陈铌陈雪芹张朋李响四川大学华西医院泌尿外科成都610041 四川大学华西医院病理研究室成都610041

目的探讨促凋亡蛋白bnip3在原发性肾透明细胞癌中的表达及其与缺氧诱导因子-1α(HIF-1α)、血管内皮生长因子(VEGF)表达的相关性。方法联合应用组织芯片技术和Envision二步免疫组化技术检测104例肾透明细胞癌及48例癌旁正常肾组织中bnip... 详细信息

目的探讨促凋亡蛋白bnip3在原发性肾透明细胞癌中的表达及其与缺氧诱导因子-1α(HIF-1α)、血管内皮生长因子(VEGF)表达的相关性。方法联合应用组织芯片技术和Envision二步免疫组化技术检测104例肾透明细胞癌及48例癌旁正常肾组织中bnip3、HIF-1α、VEGF的蛋白表达水平,并分析肾癌中bnip3表达与HIF-1α、VEGF的相关性。结果 bnip3、HIF-1α及VEGF在肾透明细胞癌中的阳性表达率分别为36.5%、61.5%和69.2%,在癌旁正常肾组织中的阳性表达率分别为12.5%、8.3%和12.5%。在bnip3阳性和阴性表达组中,HIF-1α、VEGF的阳性率之间差异无统计学意义(P>0.05),VEGF阳性组与阴性组中HIF-1α的阳性表达率差异有统计学意义(P<0.05),且两者之间的表达有相关性。结论 bnip3在透明细胞癌中有所表达,但多数为低表达,且与HIF-1α和VEGF的表达无相关性。

关键词：肾透明细胞癌 bnip3 缺氧诱导因子-1α 血管内皮生长因子细胞凋亡

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