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VEGFR2 inhibition hampers breast cancer cell proliferation via enhanced mitochondrial biogenesis

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Cancer Biology & Medicine 2021年第1期18卷 139-154页

作者： Hao Ni Min Guo Xuepei Zhang Lei Jiang Shuai Tan juan Yuan Huanhuan L Cui Yanan Min Junhao Zhang Susanne Schlisio Chunhong Ma Wangjun Liao Monica Nister Chunlin Chen Shuijie Li Nailin Li Department of Gynaecology and Obstetrics Nanfang HospitalSouthern Medical UniversityGuangzhou 510515China Karolinska Institutet Department of Medicine-SolnaClinical Pharmacology GroupKarolinska University Hospital-SolnaStockholm 17176Sweden Karolinska Institutet Department of Oncology-PathologyBio ClinicumSolna 17164Sweden State Key Laboratory of Bioorganic and Natural Products Chemistry Center for Excellence in Molecular SynthesisShanghai Institute of Organic ChemistryChinese Academy of SciencesShanghai 200032China Department of Pathology Zhejiang Provincial Key Laboratory of PathophysiologyNingbo University School of MedicineNingbo 315211China Department of Hematology Affiliated Hospital of Jining Medical UniversityJining 272000China Department of Cell and Molecular Biology Stockholm 17177Sweden Karolinska Institutet Department of MicrobiologyTumor and Cell BiologyStockholm 17177Sweden Shandong University Cheeloo Medical College School of Basic MedicineDepartment of ImmunologyJinan 250000China Department of Oncology Nanfang HospitalSouthern Medical UniversityGuangzhou 510515China

Objective:Vascular endothelial growth factor(VEGF),apart from its predominant roles in angiogenesis,can enhance cancer cell proliferation,but its mechanisms remain *** purpose of the present study was therefore to identify how VEGF regulates cancer cell ***:VEGF effects on cancer cell proliferation were investigated with the VEGF receptor 2 inhibitor,Ki8751,and the breast cancer cell lines,MCF-7 and MDA-MB-231,using flow cytometry,mass spectrometry,immunoblotting,and confocal *** were analyzed using one-way analysis of variance followed by Tukey’s multiple comparison ***:VEGF blockade by Ki8751 significantly reduced cancer cell proliferation,and enhanced breast cancer cell *** spectrometric analyses revealed that Ki8751 treatment significantly upregulated the expression of mitochondrial proteins,suggesting the involvement of mitochondrial *** microscopy and flow cytometric analyses showed that Ki8751 treatment robustly increased the mitochondrial masses of both cancer cells,induced endomitosis,and arrested cancer cells in the high aneuploid ***2 knockdown by sh RNAs showed similar effects to those of Ki8751,confirming the specificity of Ki8751 *** mitochondrial biogenesis increased mitochondrial oxidative phosphorylation and stimulated reactive oxygen species(ros)production,which induced cancer cell ***,Ki8751 treatment downregulated the phosphorylation of Akt and PGC1α,and translocated PGC1αinto the *** PGC1αalterations increased mitochondrial transcription factor A(TFAM)expression and subsequently increased mitochondrial ***:VEGF enhances cancer cell proliferation by decreasing Akt-PGC1α-TFAM signaling-mediated mitochondrial biogenesis,ros production,and cell *** findings suggested the anticancer potential of Ki8751 via increased mitochondrial biogenesis and ros production.

关键词： Breast cancer VEGF VEGFR2 mitochondria TFAM ros apoptosis

Bioactive Diarylheptanoids from Alpinia coriandriodora

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Natural Products and Bioprospecting 2021年第1期11卷 63-72页

作者： Xiao-Li Cheng Han-Xiang Li juan Chen Ping Wu Jing-Hua Xue Zhong-Yu Zhou Nia-He Xia Xiao-Yi Wei Key Laboratory of Plant Resources Conservation and Sustainable Utilization South China Botanical GardenChinese Academy of SciencesTianhe DistrictXingke Road 723Guangzhou 510650People’s Republic of China Guangdong Provincial Key Laboratory of Digital Botanical Garden South China Botanical GardenChinese Academy of SciencesXingke Road 723Tianhe DistrictGuangzhou 510650People’s Republic of China School of Life Sciences University of Chinese Academy of SciencesYuquanlu 19ABeijing 100049People’s Republic of China

Eight new diarylheptanoids,coriandralpinins A-H(1-8),were isolated from the rhizomes of Alpinia coriandriodora,an edible plant of the ginger *** structures,including the absolute configurations,were established by extensive spectroscopic analysis and ECD *** 1-8 have a 1,5-O-bridged diarylheptanoid structure featuring polyoxygenated aryl *** evaluated for intracellular antioxidant activity using t-BHP stressed RAW264.7 mac-rophages,all these compounds scavenged reactive oxygen species(ros)in a concentration-dependent *** 3 and 5 also showed inhibitory activity against NO release in LPS-induced RAW 264.7 *** known flavonols,7,4′-di-O-methylkaempferol,7-O-methylquercetin,7,4′-di-O-methylquercetin,7,3′,4′-tri-O-methylquercetin,kaempferol 3-O-β-d-(6-O-α-l-rhamnopyranosyl)glucopyranoside,and 3-O-β-d-glucopyranuronosylquercetin were also isolated and characterized from the rhizomes.

关键词： Alpinia coriandriodora Diarylheptanoid Antioxidant Anti-inflammatory

As_2O_3诱导肿瘤细胞凋亡依赖H_2O_2途径

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中国病理生理杂志 2006年第6期22卷 1185-1190页

作者：曹娟郑杰东南大学基础医学院

目的:探讨三氧化二砷(arsenic trioxide,As2O3)对人乳头瘤病毒(HPV)阳性宫颈癌HeLa细胞和HPV阴性胰腺癌AsPC-1细胞的凋亡诱导作用与细胞内H2O2水平的关系。方法:采用不同浓度的As2O3处理HeLa细胞和AsPC-1细胞不同时段,显微镜下观察细胞... 详细信息

目的:探讨三氧化二砷(arsenic trioxide,As2O3)对人乳头瘤病毒(HPV)阳性宫颈癌HeLa细胞和HPV阴性胰腺癌AsPC-1细胞的凋亡诱导作用与细胞内H2O2水平的关系。方法:采用不同浓度的As2O3处理HeLa细胞和AsPC-1细胞不同时段,显微镜下观察细胞的凋亡,噻唑蓝(MTT)法测定细胞生长抑制情况;不同浓度的As2O3处理细胞2、5、8、12、24h后,用DCFH-DA标记检测细胞内的H2O2水平。结果:2μmol/L As2O3处理HeLa细胞48h后细胞的生长受到明显抑制,表现出细胞凋亡的特征,随着As2O3浓度的增加和作用时间的延长效果更加明显。而1μmol/L As2O3处理AsPC-1细胞24h即呈现明显的生长抑制和凋亡特征。As2O3处理HeLa细胞2h细胞内H2O2的水平比对照组升高(10μmol/L组达51·30%),持续到8h达到高峰(升高84·19%),12h后下降,24h水平与对照组接近,并有明显的剂量依赖性。As2O3处理AsPC-1细胞2h后,细胞内H2O2的水平也明显升高(10μmol/L组达79%),持续到5h达到高峰(增高169%),且该细胞内H2O2水平升高比HeLa细胞更明显,12h之后的变化情况与HeLa细胞类似。结论:As2O3诱导HeLa细胞和AsPC-1细胞凋亡与细胞内的H2O2水平改变有关,而与HPV的感染无明显相关性。H2O2积累是As2O3诱导细胞凋亡途径中的早期事件,H2O2可能在As2O3诱导肿瘤细胞凋亡途径中扮演类似第二信使的作用。

关键词：三氧化二砷肿瘤细胞凋亡活性氧 HeLa细胞

阿魏酸预处理对阿霉素诱导H9c2心肌细胞损伤的保护作用

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中国药理学通报 2014年第8期30卷 1059-1065页

作者：吴枝娟余靖王瑞幸方秋娟林默君福建医科大学基础医学院生理学与病理生理学系福建福州350108

目的研究阿魏酸(FA)对阿霉素(DOX)诱导H9c2心肌细胞损伤的影响。方法 1μmol·L-1DOX处理H9c2细胞24 h,建立心肌损伤模型。FA预处理组,10、20、40μmol·L-1FA预处理2 h后,再与DOX共培养24 h。CCK-8比色法测定细胞生存率;相差显微镜观... 详细信息

目的研究阿魏酸(FA)对阿霉素(DOX)诱导H9c2心肌细胞损伤的影响。方法 1μmol·L-1DOX处理H9c2细胞24 h,建立心肌损伤模型。FA预处理组,10、20、40μmol·L-1FA预处理2 h后,再与DOX共培养24 h。CCK-8比色法测定细胞生存率;相差显微镜观察细胞形态学改变;生化试剂盒检测LDH、CK、MDA、SOD;DCF-DA荧光染色流式细胞术检测细胞内活性氧;AO-EB染色、DNA琼脂糖凝胶电泳检测细胞凋亡;Western blot法测定caspase-3、Bax、Bcl-2表达。结果 DOX降低H9c2细胞生存率,诱导氧化应激损伤和细胞凋亡。FA预处理剂量依赖性提高细胞生存率,减轻LDH、CK外漏和损伤细胞形态学改变。FA减少ros生成,降低细胞MDA水平,增加SOD酶活性,抑制DOX诱导的氧化应激。FA下调促凋亡蛋白caspase-3和Bax,上调凋亡抑制蛋白Bcl-2,减少心肌细胞凋亡。结论 FA可抑制DOX诱导的氧化应激和心肌细胞凋亡,减轻心肌损伤。

关键词：阿魏酸阿霉素心肌保护 H9 c2心肌细胞凋亡氧化应激

A chemical genetic approach clarifies MPK3/MPK6 activation and NADPH oxidase-mediated oxidative burst in plant immunity are two independent signaling events in plant immunity

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A chemical genetic approach clarifies MPK3/MPK6 activation a...

抑制或过表达GRK5基因对星形胶质细胞凋亡及IL-1β和TNF-α表达的影响

2013全国植物生物学大会

作者： XU juan XIE Jie LIU Yidong ZHANG Shuqun College of Life Sciences Zhejiang University Department of Biochemistry University of MissouriColumbiaMissouriUSA

Arabidopsis thaliana MPK3 and MPK6,two closely related MAPKs with functional redundancy,are key players in regulating multiple defense ***3/MPK6 can be activated by various stimulus and are involved in including ethylene induction,phytoalexin biosynthesis, defense gene activation,reactive oxygen species(ros)generation, hypersensitive response(HR) cell death,and disease resistance by phosphorylating different substrates including ACS2/ACS6,WRKY33,and *** recognition of pathogen-associated molecular patterns(PAMPs) such as bacterial flagellin-derived fig22 triggers the generation of reactive oxygen species(ros) and the rapid activation of at least three different MAPKs,MPK3,MPK6 and ***,the relationship between the flg22-activated MAPKs and induced ros burst has been a controversial issue because of the lacking of detailed genetic *** redundancy and embryo lethality of the mpk3 mpk6 double mutant make it difficult to clarify their roles in a specific signaling *** a chemical genetic approach,we generated a new conditional loss-of-function mpk3 mpk6 double mutant in which the activity of MPK3 and MPK6 can be inhibited by the application of NA-PP1 inhibitor at the required *** with the conditionally rescued mpk3 mpk6 double mutant reported previously,we demonstrate that flg22-triggered ros burst is independent of MPK3/ *** Arabidopsis mutant lacking a functional AtRbohD,flg22-induced ros burst was completely ***,the activation of MPK3/MPK6 was not *** on these results,we conclude that the rapid ros burst and MPK3/MPK6 activation are two independent early signaling events downstream of FLS2 in plant *** contrast,MPK4 has a negative impact on the flg22-induced ros *** addition,salicylic acid-pretreatment enhances AtRbohD-mediated ros burst,which is again independent of MPK3/MPK6 based on the analysis of the newly generated mpk3 mpk6 double *** establishment of the

关键词： MPK3/MPK6 activation chemical genetic approach plant immunity ros burst mpk3 mpk6 double mutant

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中国免疫学杂志 2018年第8期34卷 1163-1167页

作者：贾蕾史娟延安大学附属医院神经内科延安716000 延安大学医学院

目的:探讨抑制或过表达G蛋白偶联受体激酶5(GRK5)基因对星形胶质细胞(AS)凋亡及IL-1β和TNF-α表达的影响。方法:培养原代AS,将干扰GRK5表达的siRNA(GRK5-siRNA)及GRK5的过表达质粒(pc DNA3.1-GRK5)分别转染AS,通过Western blot检测转染... 详细信息

目的:探讨抑制或过表达G蛋白偶联受体激酶5(GRK5)基因对星形胶质细胞(AS)凋亡及IL-1β和TNF-α表达的影响。方法:培养原代AS,将干扰GRK5表达的siRNA(GRK5-siRNA)及GRK5的过表达质粒(pc DNA3.1-GRK5)分别转染AS,通过Western blot检测转染24 h后的细胞中GRK5蛋白的表达;缺氧处理AS,细胞分为空白组、缺氧组、缺氧+pc DNA3.1-GRK5组和缺氧+GRK5-siRNA组,缺氧处理24 h后通过流式细胞仪检测各组细胞的凋亡率及ros含量;RT-PCR检测IL-1β和TNF-α的mRNA表达;Western blot检测p53、信号转导与转录因子3(STAT3)和p-STAT3蛋白表达。结果:与空白组比较,转染GRK5-siRNA的AS中GRK5的表达显著降低,转染pc DNA3.1-GRK5的细胞GRK5的表达显著升高(Pros水平及IL-1β、TNF-α、p53和p-STAT3的表达均显著升高(Pros水平及IL-1β、TNF-α、p53和p-STAT3的表达均显著降低,缺氧+GRK5-siRNA组细胞凋亡率、ros水平及IL-1β、TNF-α、p53和p-STAT3的表达均显著升高(Pros水平,下调IL-1β、TNF-α、p53表达及STAT3信号通路,抑制GRK5表达反之。

关键词： GRK5基因星形胶质细胞凋亡 STAT3信号通路 IL-1β TNF-α

Artemisinin inhibits inflammatory response via regulating NF-κB and MAPK signaling pathways

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Artemisinin inhibits inflammatory response via regulating NF...

The expression of SIRT3 signaling in hypoxia-induced endothelial injury

中国化学会第十一届全国天然有机化学学术会议

作者： Ke Si Wang Chunliu Mi juan Ma Xuejun Jin Key Laboratory of Natural Resources of Changbai Mountain ＆ Functional Molecules Ministry of education Molecular Medicine Research Center College of Pharmacy Yanbian University

Artemisinin, isolated from the Chinese plant Artemisia annua, has been used for many years to treat different forms of malarial parasites. In this study, we explored the antiinflammatory activity of artemisinin and the underlying mechanism of this action. We demonstrated that the anti-inflammatory effects of artemisinin in TPA-induced skin inflammation in mice. Then the artemisinin significantly inhibited the expression of NF-κB reporter gene induced by TNF-α in a dose-dependent manner. Artemisinin also inhibited TNF-α induced phosphorylation and degradation of IκBα, p65 nuclear translocation. Furthermore, pretreatment of cells with artemisinin prevented the TNF-α-induced expression of NF-κB target genes, such as anti-apoptosis（c-IAP1, Bcl-2, and FLIP）, proliferation（COX-2, cyclin D1）, invasion（MMP-9）, angiogenesis（VEGF）, and major inflammatory cytokines（TNF-α, i NOS, and MCP1）. We also proved that artemisinin potentiated TNF-α-induced apoptosis. Moreover, artemisinin significantly impaired the ros production and phosphorylation of p38 and ERK, but did not affect the phosphorylation of JNK. Taken together, artemisinin may be a potentially useful therapeutic agent for inflammatory-related diseases.

关键词： Artemisinin Inflammation Nuclear factor-κB(NF-κB) IκBα MAPK

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South China Journal of Cardiology 2020年第4期21卷 277-284页

作者： CHEN Chun-juan LIN Mei-ling WANG Wei YU Wei Department of Cardiology Second Affiliated Hospital of Shantou University Medical CollegeShantou 515041China Department of Cardiology First Affiliated Hospital of Shantou University Medical CollegeShantou 515041China Department of Internal Medicine Xiang'an Hospital of Xiamen UniversityXiamen 361102China

Background Oxidative injury to the endothelial cells plays an important role in development of *** of the mechanisms of oxidative endothelial injury is of great *** previous report has demonstrated that Sirtuin 3(SIRT3)protect cardiomyocytes from oxidative stress-mediated cell death via activating the nuclear factor kappa-B(NF-κB)signaling ***,the role and exact mechanisms of SIRT3 signaling in endothelial hypoxia injury are largely *** present study aimed to investigate the expression of SIRT3,hypoxia-inducible factor 1α(HIF-1α),and NF-κB/TNF-α(tumor necrosis factor-α)in human umbilical vein endothelial cells(HUVECs)treated by *** Hypoxia model was established by anoxic tank and randomly divided into 3 groups:control group,1 h hypoxia group,and 3 h hypoxia group.3-(4,5-dimetrylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT)detected the cell viability under hypoxia condition,and the intracellular reactive oxygen species(ros)generation was determined by 2′,7′-Dichlorodihydrofluorescein diacetate(DCFH-DA).The expression of m RNA and protein of the SIRT3 signaling were detected by real-time quantitative polymerase chain reaction(q PCR)and western blot analysis,*** Hypoxia treatment time-dependently decreased the cell viability,especially in the first *** production significantly increased in the first hour of hypoxia compared with those in the second and the third *** stimuli significantly elevated SIRT3 m RNA and protein ***,real-time q PCR results showed that elevated SIRT3 significantly increased the m RNA expression of HIF-1αand NF-κB/TNF-αin 1 h hypoxia *** blot results also showed that elevated SIRT3 significantly increased the protein expression of NF-κB in the 1 h hypoxia *** The present study indicated that hypoxic stimuli promoted the expression of SIRT3,HIF-1α,and NF-κB/TNF-α,and suggested that SIRT3 signaling path

关键词： hypoxic injury human endothelial cells signaling pathway SIRT3

顺铂联合小檗碱通过诱导DNA损伤和ros依赖性凋亡抑制肺癌细胞A549的生长

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中国药理学通报 2020年第6期36卷 844-851页

作者：毛娟娟程伟松杨亦德金茜汪佳兵台州市立医院感染科浙江台州318000 台州市立医院泌尿外科浙江台州318000 台州市立医院药剂科浙江台州318000

目的探究顺铂联合小檗碱(berberine,BBR)对人肺癌A549细胞增殖、凋亡的作用及抗肺癌机制。方法MTT法分别检测不同浓度的BBR、BBR联合不同浓度的顺铂对A549细胞增殖的作用;设置溶剂组、顺铂组、小檗碱组和顺铂+小檗碱组,细胞集落实验检... 详细信息

目的探究顺铂联合小檗碱(berberine,BBR)对人肺癌A549细胞增殖、凋亡的作用及抗肺癌机制。方法MTT法分别检测不同浓度的BBR、BBR联合不同浓度的顺铂对A549细胞增殖的作用;设置溶剂组、顺铂组、小檗碱组和顺铂+小檗碱组,细胞集落实验检测细胞集落形成;流式细胞术实验检测细胞凋亡;Western blot检测Bcl-2、cleaved-caspase-3及γH2AX蛋白表达;免疫荧光实验检测DNA损伤;活性氧(reactive oxygen species,ros)清除剂N-乙酰半胱氨酸(N-acetyl-L-cysteine,NAC)预处理后,流式细胞术实验和Western blot分别检测ros水平和Bcl-2、cleaved-caspase-3蛋白表达。结果BBR及BBR联合顺铂浓度依赖性抑制A549细胞生长(Pros水平(Pros介导Bcl-2和cleaved-caspase-3蛋白表达有关。

关键词：顺铂小檗碱 A549细胞凋亡 DNA损伤 ros