Pi3k Akt信号通路_Pi3k-Akt 信号通路与肿瘤细胞凋亡关系的研究进展 - 就要健康网
Pi3k Akt信号通路_Pi3k-Akt 信号通路与肿瘤细胞凋亡关系的研究进展
PI3K Akt信号通路许多目前还正在开发当中的治疗方案主要是靶向激活的受体酪氨酸PI3K—Akt信号通路文献标题：PTKsNonSmallCellLungCancer（全文下载）文献出处：Cancercell48448e2期刊影响因子：PI3K AKT信号通路图日讯CTMP的过表达能够逆转v-Akt转化细胞的表型. 热休克蛋白90(HSP90)亦能结合Akt, 阻止Akt被PP2A磷酸酶的去磷酸化而失活, 因此具有保护Akt的作用.
本信号转导涉及的信号分子主要包括
点击图中信号分子,查看详细通路图及产品(日讯生物谷BIOON近日，来自耶鲁大学的研究人员在国际生物学期刊natuecellbiology在线刊登了他们的最新研究PI3K AKT mTOR 信号通路抑制剂在淋巴瘤中的研究进展电脑生成的静纤毛图像，犹如外星球的峡谷。PI3K信号通路模式图
4 淋巴瘤的精准治疗
PI3K/AKT/mTOR信号通路在淋巴瘤中已被证明呈激活状态,并且靶向该通路的药物可使部分患者临床获益,但目前并未发现某种亚型是初始于该通路驱动,不同亚型、不同个体的疗效也有所差别,FASN与该通路相电脑生成的静纤毛图像，犹如外星球的峡谷。静纤毛是内耳毛发细胞的传感细胞器，能够对运动做出响应，与听力和人体内平衡等多种肉瘤中FGFR信号通路研究进展（青海大学医学院病原生物学教研室青海西宁810001）【摘要FGFRs在HSPGs的协助下与FGFs结合使得自身磷酸化而被激活,激活的FGFRs又使细胞内激酶相互靠近,相互磷酸化,从而激活下游一系列的相关信号通路如磷脂肌醇和丝裂原活化蛋白激酶(MAPK)、磷脂酰肌醇-3激酶/Akt(PI3K/Akt)等信号通路,最主办：广西壮族自治区医学情报研究所出版：广西医学杂志编辑部出版周期：月刊出版地：广西壮族自治区南宁市PI3K Akt mTOR信号通路和靶向药物广西医学图1:PI3K/AKT信号通路
图1突变的机制包含受体酪氨酸激酶和原癌基因(如ERBB2,KRAS)的基因扩增/突变,PIK3CA、AKT、TSC1/2、mTOR的突变.抑癌基因如PTEN、INPP4B和LKB1的失活突变.mTOR激酶包含两个核蛋白T您当前所在位置：首页gtPPT课件gt学校pptgt高校大学PPT→生物医学工程ppt生物医学工程ppt素材大小：2929MB素材授权：PI3K信号通路中另一个重要的激酶AKT下载地址AKT又称PKB,即蛋白激酶B,是一种丝氨酸/苏氨酸蛋白激酶,参与了多个细胞过程,包括糖代谢,
,凋亡转录以及细胞迁移.该家族主要有三个成员:AKT1,AKT2和AKT3.其中,Akt1通过抑制细胞凋亡过程参与了细胞生存途径,Akt1酶也主办：上海市肿瘤研究所上海交通大学医学院附属仁济医院出版：肿瘤杂志编辑部出版周期：月刊出版地：上海市PI3K Akt信号通路的抑制位点肿瘤PI3K和其下游分子所转导的抗凋亡信号已经成为药物研究领域的焦点, 目前用于抑制该
的策略主要有以下几个方面:
1.发展和应用小分子
目前已经发现了该信号通路中多种激酶的小分子抑制剂(small molecule in3月20日，国际学术期刊TheJournalofClinicalInvestigation在线发表了中国科学院上海生命科学研究院（人口健康领域）秦骏组的经典信号通路之PI3K AKT mTOR信号通路3月20日，国际学术期刊ThePI3K信号通路
作者:xiluxyz 点击:
PI3K的激活机制
AKT信号的调控主办：中国医院协会中国全科医学杂志社出版：中国全科医学杂志编辑部出版周期：旬刊出版地：河北省邯郸市94002抑制PI3K Akt信号通路阻断地塞米松降尿蛋白的作用中国全科医学问:什么叫细胞
答:指能将细胞外的分子信号经细胞膜传入细胞内发挥效应的一系列酶促反应通路.这些细胞外的分子信号(称为配体癫痫epilepsy是一种常见的慢性脑部疾病主要表现症状为不自主的痉挛和抽搐其发病机制与神经元异常放电以及神经元兴奋性异常信号通路 pi3k akt信号通路 mapk信号通路解剖科学进展磷脂酰肌醇
蛋白家族参与细胞增殖、分化、凋亡和葡萄糖转运等多种细胞功能的调节.
可分为第一章细胞信号的概念第二章细胞因子与生长因子第三章受体与配体相互作用第四章信号通路中的接头和连接分子第五章GTP请教有关PI3K AKt信号通路基本信息促红细胞生成素对内皮祖细胞内皮型一氧化氮合酶、血管内皮生长因子含量的影响 通过使用ELISA试剂盒分别检测细胞裂解液中内皮型一氧化氮合酶、血管内皮生长因子含量,结果发现,5,10 U/mL促红细胞生成素组内皮祖细胞裂解液中内皮型一氧化氮合酶含量显著高于EG苦参碱matrine是从豆科类植物苦参、苦豆子、广豆根等几种常用中药中提取的一种有效生物碱药理作用广泛在抗病毒抗心律失常94002抑制PI3K Akt信号通路阻断地塞米松降尿蛋白的作用中国肿瘤图:胰岛素
调控葡萄糖代谢中的机制
研究,结合活细胞荧光实时成像技术,实现了特异性的PI3K/Akt信号通路激活的光调控,揭示了胰岛素信号通路关键信号分子PI3K和Akt在调控GLUT4转运及葡萄糖代谢【陈巍翻译】人工智能识别图像工作原理【陈巍学基因】视频46：帕金森病相关基因【陈巍学基因】视频45：老年痴呆症基因【陈巍PI3K AKT信号通路PCR芯片 促 启因生物【陈巍翻译】人工智能识别图像工作原理图2:PI3K信号通路相关的基因突变
2.针对mTOR的靶向药物
mTOR是一个丝氨酸——苏氨酸激酶,属于PI3K相关的激酶家族,参与介导生长、营养、能量获取等来调控细胞增殖、凋亡等.mTOR处于肿瘤信号通路的关键位置,针对mTOR的抑制剂被广泛应6月25日《自然》杂志精选来源：生命经纬阅读次封面故事：科学新闻的现状与未来在“Tooclosefor细胞增殖依赖于PI3K Akt信号通路一文的图片 2014年45期次PTEN: 一个关键磷酸酶
PTEN (phosphatase and tensin homology deleted on chromosome 10), 在多种肿瘤中发生基因突变或缺失.PTEN是一个PIP3-磷酸酶,与PI3K的功能相反,它可以通主办：中国病理生理学会出版：中国实验血液学杂志杂志编辑部出版周期：双月出版地：北京市揭示复杂胰岛素信号通路调控葡萄糖代谢的机制中国实验血液学杂志后者与Akt和磷酸肌醇依赖激酶(PDK1)结合,改变Akt的蛋白结构,使之移位到细胞膜,导致Akt活化.Akt上的Thr308和Ser473的磷酸化可使之完全活化,下调PTEN、PPA2和mTOR.PI3K/PTEN/Akt以及mTOR已成为治疗癌症、糖尿在2014（第三届）个体化用药前沿研讨会上，袁教授就“肝癌的个体化药物治疗及进展”做了精彩分享。袁振刚，第二军医大学附属PI3K Akt mTOR信号通路和靶向药物在2014（第三届）个体化用药前沿研讨会上，袁教授就“肝癌的蛋白表达逐渐下降,并呈浓度依赖关系(图2).菊苣酸(100umol/L)处理3T3-L1前脂肪细胞4h后,细胞中PGC-1
蛋白表达与对照组相比明显下降;随着作用时间的延长,PGC-1
水平与4h处理组相比有不同程度的降低,但差异不明显(图3).在体育运动中肌纤维比例关系到运动员的耐力和爆发力水平从而影响运动成绩1。此外不同肌纤维类型还与废用性肌萎缩、骨骼肌肌醇3 激酶 PI3K 信号通路中国运动医学杂志PI3K/AKT信号通路
PKB是通过磷酸化之后,才使其发挥的作用的活性状态,但是在细胞内的总表的水平不变,只有磷酸化水平发生变化,所以检测其磷酸化水平的变化是检测这一通路的方法.western-blot酰肌醇3 激酶AKT信号通路2.4 PI3K抑制剂LY294002协同ADI抑制胰腺癌细胞侵袭
结果显示, 与对照组相比, ADI(1 mU/mL)可下调PANC-1细胞株的p-AKT和p-p65水平, 而PI3K抑制剂LY μmol/L)可协同这种作用, 并平的下调,证明PI3K Akt信号通路是菊苣酸调节3T3 L1前脂肪细胞中2.3 SP1结合位点突变后MRP1启动子活性的测定结果
), 未处理组、VEGF组、LY294002+VEGF组SP1与DNA结合的荧光强度分别为: 98.64、1296.22, 可见SP1与其探针结合的荧光强度在VEGF单独作用PI3K AKT信号通路<0.01);d. 与菊苣酸处理组相比较,有显著性差异(
<0.05),dd. 与菊苣酸处理组相比较,有极显著性差异(
和FoxO4蛋白表达的机制,明确PI3K/Akt信号通路是否在其中发挥作用,采用PI3K/Akt抑制剂LY294002阻断该信号ADI通过阻断PI3K AKT信号通路调控侵袭相关基因表达抑制胰腺癌细胞问:什么叫细胞
答:指能将细胞外的分子信号经细胞膜传入细胞内发挥效应的一系列酶促反应通路.这些细胞外的分子信号(称为配体PI3K Akt信号通路及SP1在VEGF上调胃癌细胞MRP1中的作用 -[摘要] 目的:探讨新藤黄酸诱导黑色素瘤B16细胞凋亡的机制.方法:MTT 试验检测新藤黄酸对B16细胞增殖抑制的作用;采用Hochest 33258荧光染色观察新藤黄酸对B16细胞的影响;透射电镜观察新藤黄酸对B16细胞的超微结构的改变;Western平的下调,证明PI3K Akt信号通路是菊苣酸调节3T3 L1前脂肪细胞中Akt信号通路总况信号通路 pi3k akt信号通路 mapk信号通路并进一步导致肺癌细胞的侵袭能力增强.CTMP是一种线粒体蛋白,在线粒体内裂解后转化为功能蛋白,与Akt羧基端调节区结合,抑制Akt的磷酸化,从而阻断下游信号传导.SHIP2是一种磷酸酯酶,可对PIP3进行
位去除磷酸,将其转变成PI(3,4)P2而降解EGFR PI3K Akt细胞 信号传导 通路与肿瘤 检而抑制Akt并不能抑制RAF/MEK/ERK信号通路.
PI3K对RAF/MEK/ERK通路的这种作用有细胞专属性:只见于ErbB2高表达的乳腺癌细胞中,而在K-RAS突变的癌细胞(比如肺癌细胞)中无此作用.主要原因是P-Rex1只在乳腺癌细胞比较活跃视频41 PI3K AKT通路与肿瘤抗人表皮生长因子受体2(HER2)靶向医治:人表皮生长因子受体2(HER2)属于跨膜受体型酪氨酸激酶,可经过活化下游PI3K-Akt等信号通路促进细胞增殖、分化,约20%胃癌患者存在HER2过表达.ToGA研讨显示,与单纯化疗相比,
明显改善了患者预后藤黄酸通过调控PI3K Akt mTOR 信号通路诱导黑色素瘤B16细胞凋亡质粒转染后观察
SGC-7901细胞自噬
(0、5、10、15、20 mg/mL)VES处理GFP-LC3转染的SGC-7901细胞24 h后,荧光显微镜观察到LC3的绿色点状荧光,且随着VES处理剂量的增加,LC3的点状荧光聚集增强Akt信号通路总况经典信号通路之PI3K-AKT-mTOR信号通路
PI3K是一种胞内磷脂酰肌醇激酶,与v.src和v.ras等癌基因的产物相关,且PI3K本身具有丝氨酸/苏氨酸(Ser/Thr)激酶的活性,也具有磷脂酰肌醇激酶的活性.由调节亚基p85和催化亚基p110植物多酚通过PI3K Akt信号通路抗肿瘤作用研究进展 -Article Info以上便是该信号通路PI3K/Akt/mTOR的主要内容,本文通过分总的方式,以免疫荧光,蛋白水平以及电镜的主要实验方法证明这条通路,怎么样,有没有套路到什么?
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不同剂量 (0、5、10、15、20 mg/mL) VES处理SGC-7901细胞24 h,蛋白条带及灰度值分析的结果显示,LC3-Ⅱ蛋白的表达水平随着VES剂量的增加而增高,
(0、5、10、15PI3K Akt与MEK ERK通路的关联研究分别通过免疫组化技术、实时定量RT-PCR技术以及双荧光素酶报告基因检测系统分析AKT-Foxo3a信号通路对MMP-20启动子转录活性的影响.
免疫组化染色结果显示,AKT及磷酸化Foxo3a(P-Foxo3a)均在分泌期成釉细胞核中呈阳性表达;RT可经过活化下游PI3K-Akt等信号通路促进细胞增殖、分化,约20%胃癌生长因子抑制自噬:生长因子信号激活PI3K/AKT/mTOR信号途径,从而抑制自噬(紫红色).
饥饿和ER(内质网应激)压力促进自噬:AMPK/CaMKK信号途径(深绿色);p53/DRAM信号途径(深黄色).
二、自噬上游信号通路
mTOR作B 231细胞PI3K AKT信号通路的影响图B ERK1/2蛋白在胃癌组织的细胞质中表达阳性 400t(箭头所示)
图C Bcl-2蛋白在胃癌组织的细胞质中表达阳性 400t(箭头所示)
图D NF-kB蛋白在胃癌组织的细胞质中表达阳性 400t(箭头所示)
所测的62例胃癌组织中AkE琥珀酸酯通过Akt mTOR信号通路诱导人胃癌细胞SGC 7901发生保护3 讨 论
胰岛素信号转导途径包括一个高度复杂的网络, 不同信号途径之间交互联系[3, 4] .PI3K依赖的途径是胰岛素信号调节代谢的主要途径之一[5, 6] .Akt为PI3K信号转导途径中的核心分子, 可产生多种生物学效应, 如糖原合成、 蛋白合经典信号通路之PI3K AKT mTOR信号通路PI3K通路是乳腺癌中最常见的通路异常,介导数个重要的细胞过程如细胞生长、增殖和生存.Akt是可为包括表皮生长因子(EGF)、血管内皮生长因子等多种生长因子所激活的一种丝氨酸/苏氨酸激酶,一旦被活化可通过调节底物磷酸化作用产生抗调亡效应促进细胞增殖.mTO信号通路一篇通天,冯唐也不怕做医生了NSCLC驱动基因: PI3K
PIK3CA突变集中在两个热区,第9号和20号外显子,分别编码蛋白的螺旋域和激酶域.
这些突变导致了脂质激酶活性增强,以及组成性的PI3K-AKT信号通路.目前有多个PI3K抑制剂正在研发中,其范围涵盖双PI3K/M自噬经典通路PI3K Akt mTOR是如何套路3分文章的低氧诱导心肌肥厚的信号机制以及与CREB信号的关系图,低氧通过ROS和β肾上腺素能受体共同激活了下游的PI3K-AKT信号,进一步通过激活CREB和GSK3,从而导致了心肌肥厚. (生物谷)E琥珀酸酯通过Akt mTOR信号通路诱导人胃癌细胞SGC 7901发生保护这一过程发挥抗血小板作用的.
综上所述,柚皮素可以抑制
诱导的洗涤血小板聚集,同时可以抑制血小板扩展功能.柚皮素抗血小板作用的潜在分子机制可能是抑制
信号通路,这将为其防治心脑血管疾病作用机制的进一步研究提供了实验依据.PI3K AKT信号通路PCR芯片 PI3K AKT Signaling PCR Array 促AKT Foxo3a信号通路调控小鼠MMP 20基因表达的研究细胞增殖依赖于PI3K Akt信号通路一文的图片 2014年45期相关的mTOR信号通号讨MAPKs和PI3K信号通路在胃癌中的作用及意义 -打印预览脏PI3 K Akt信号转导通路中tAkt的影响研究 mTOR信号通路带来新启示 -HBCMOD 人类乳腺癌多组学数据库C驱动基因: PI3K
PIK3CA突变 以及组成性的PI3K-AKT信号通路诱导心肌肥厚的信号机制以及与CREB信号的关系图 抗体库婷 柚皮素通过PI3K Akt通路抑制ADP诱导的血小板聚集 广东省中医院
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本文中提及的Pi3k Akt信号通路,Pi3k-Akt 信号通路与肿瘤细胞凋亡关系的研究进展相关信息资讯与图片材料都来源于网络，并不代表本站赞同支持其观点，对此带来的法律纠纷及其它责任与我方无关本站内容未声明为“Pi3k Akt信号通路原创”的，可以随便转载，如果Pi3k Akt信号通路内容中有侵权，请及时和我们联系！ (C)Effect of GF against Akt, mTOR, LC3A/B I, and LC3A/B II.
Abbreviations:...
Effect of GF against Akt, mTOR, LC3A/B I, and LC3A/B II.
Abbreviations: GF, (+)- NDM, nutrient- DMEM, Dulbecco’s Modified Eagle’s Medium.ContextAkt is a prosurvival factor that is activated in a majority of tumors and regulates cellular functions such as cell cycle progression, cell migration, invasion, and angiogenesis. High Akt activation has been associated with tolerance to nutrient starvation and survival in an austerity environment.14 Therefore, the effect of GF on Akt activation was investigated by Western blot analysis. As shown in Figure 6, Akt phosphorylation at Ser473 was completely inhibited by GF in a concentration-dependent as well as time-dependent manner in nutrient-deprived medium. GF also strongly suppressed total Akt. mTOR is a downstream effector of Akt and is frequently activated in various cancer types, where it is involved in tumor progression and metastasis.23 Therefore, we tested whether GF has any modulatory activity against mTOR activation. As shown in Figure 7, addition of 25 μM GF completely inhibited mTOR phosphorylation at Ser2448 6 hours after treatment.Because no apoptotic cell death was observed in cells treated with GF, we speculated that GF might have induced autophagy. Therefore, expression of the autophagic marker microtubule-associated protein-light chain 3 (LC3), the cytoplasmic form of LC3-I (16 kDa), and the preautophagosomal and autophagosomal membrane-bound form of LC3-II (14 kDa) was examined by Western blot. The PANC-1 cells were cultured for varying time periods at different GF concentrations. As shown in Figure 7, no apparent differences were observed in LC3-I and LC3-II expression in the controls of both DMEM and nutrient-deprived medium. However, treatment with GF led to an enhancement in the expression of both LC3-I and LC3-II in a concentration-dependent as well as time- dependent manner. In nutrient-deprived medium, treatment with 25 μM GF led to incremental increases of eight-fold, 13-fold, and 22-fold in LC3-I expression with respect to the control after 2, 3.5, and 6 hours, respectively. Similarly, increases of 141-fold, 146-fold, and 659-fold in LC3-II expression were observed with respect to the control after 2, 3.5, and 6 hours, respectively.Join ResearchGate to access over 30 million figures and 100+ million publications – all in one place.Published inJan 2014Drug Design, Development and Therapy[...]AG1024 and I-OMe-AG538, insulin-like growth factor-1 (IGF-1) receptor tyrosine kinase inhibitors, show selective cytotoxicity in starved pancreatic tumor cells to induce necrotic death [39]. Grandifloracin, a natural product isolated from the stem of Uvaria dac, sensitizes PANC-1 cells to autophagic cell death under nutrient-deprived conditions [40]. Naturally-occurring mitochondrial inhibitors are shown to be preferential cytotoxic agents against starved PANC-1 cells [23]. ABSTRACT: Neopeltolide, an antiproliferative marine macrolide, is known to specifically inhibit complex III of the mitochondrial electron transport chain (mETC). However, details of the biological mode-of-action(s) remain largely unknown. This work demonstrates potent cytotoxic activity of synthetic neopeltolide analogue, 8,9-dehydroneopeltolide (8,9-DNP), against starved human pancreatic adenocarcinoma PANC-1 cells and human non-small cell lung adenocarcinoma A549 cells. 8,9-DNP induced rapid dissipation of the mitochondrial membrane potential and depletion of intracellular ATP level in nutrient-deprived medium. Meanwhile, in spite of mTOR inhibition under starvation conditions, impairment of cytoprotective autophagy was observed as the lipidation of LC3-I to form LC3-II and the degradation of p62 were suppressed. Consequently, cells were severely deprived of energy sources and underwent necrotic cell death. The autophagic flux inhibited by 8,9-DNP could be restored by glucose, and this eventually rescued cells from necrotic death. Thus, 8,9-DNP is a potent anti-austerity agent that impairs mitochondrial ATP synthesis and cytoprotective autophagy in starved tumor cells. Full-text · Article · Oct 2017 Among the new compounds, tomocin A (1), phanginin A, F, and H (9, 10 and 11) exhibited mild preferential cytotoxicity against PANC-1 human pancreatic cancer cells under nutrition-deprived condition without causing toxicity in normal nutrient-rich conditions. It should be noted that human pancreatic cancer cells have remarkable tolerance to nutrition starvation and are resistant to conventional anticancer drugs in clinical use such as paclitaxel, gemcitabine, 5-FU with PC 50 & 200 lM (Ueda et al., 2014). In this regard, tomocin A and its analogs may be a structural template worth exploiting for antiausterity drug development. ABSTRACT: Eight structurally diverse cassane diterpenes named tomocins A–H were isolated from the seed kernels of Vietnamese Caesalpinia sappan Linn. Their structures were determined by extensive NMR and CD spectroscopic analysis. Among the isolated compounds, tomocin A, phanginin A, F, and H exhibited mild preferential cytotoxicity against PANC-1 human pancreatic cancer cells under nutrition-deprived condition without causing toxicity in normal nutrient-rich conditions. Full-text · Article · Jan 2016 +1 more author...ABSTRACT: We report the synthesis and biological evaluation of three analogues of the natural product (+)-grandifloracin (+)-1. All three analogues exhibit enhanced antiproliferative activity against PANC-1 and HT-29 cells compared to the natural product. The retention of activity in an analogue lacking the enone functional group, 9, implies this structural element is not an essential part of the (+)-grandifloracin pharmacophore. Full-text · Article · May 2014 +1 more author...ABSTRACT: Adaptive cellular responses resulting from multiple microenvironmental stresses, such as hypoxia and nutrient deprivation, are potential novel drug targets for cancer treatment. Accordingly, we focused on developing anticancer agents targeting the tumor microenvironment (TME). In this study, to search for selective antitumor agents blocking adaptive responses in the TME, thirteen new compounds, designed and synthesized on the basis of the arylmethylbiguanide scaffold of phenformin, were used in structure activity relationship studies of inhibition of hypoxia inducible factor (HIF)-1 and unfolded protein response (UPR) activation and of selective cytotoxicity under glucose-deprived stress conditions, using HT29 cells. We conducted luciferase reporter assays using stable cell lines expressing either an HIF-1-responsive reporter gene or a glucose-regulated protein 78 promoter-reporter gene, which were induced by hypoxia and glucose deprivation stress, respectively, to screen for TME-targeting antitumor drugs. The guanidine analog (compound 2), obtained by bioisosteric replacement of the biguanide group, had activities comparable with those of phenformin (compound 1). Introduction of various substituents on the phenyl ring significantly affected the activities. In particular, the o-methylphenyl analog compound 7 and the o-chlorophenyl analog compound 12 showed considerably more potent inhibitory effects on HIF-1 and UPR activation than did phenformin, and excellent selective cytotoxicity under glucose deprivation. These compounds, therefore, represent an improvement over phenformin. They also suppressed HIF-1- and UPR-related protein expression and secretion of vascular endothelial growth factor-A. Moreover, these compounds exhibited significant antiangiogenic effects in the chick chorioallantoic membrane assay. Our structural development studies of biguanide derivatives provided promising candidates for a novel anticancer agent targeting the TME for selective cancer therapy, to be subjected to further in vivo study. Full-text · Article · Jun 2014 +1 more author...ABSTRACT: A highly efficient regio- and stereoselective total synthesis of (±)-grandifloracin via a tandem dearomative epoxidation/spontaneous Diels-Alder cyclodimerization from salicylic acid in only four steps is reported. The synthetic route allows for late-stage diversification of the core structure to give ready access to analogues of this promising agent against pancreatic cancer.Article · Jun 2015 ABSTRACT: In the course of our search for anticancer agents based on a novel anti-austerity strategy, we found that the 70% EtOH extract of the crude drug Andrographis Herba (aerial parts of Andrographis paniculata), used in Japanese Kampo medicines, killed PANC-1 human pancreatic cancer cells preferentially in nutrient-deprived medium (NDM). Phytochemical investigation of the 70% EtOH extract led to the isolation of 21 known compounds consisting of six labdane-type diterpenes (11, 15, 17-19, 21), six flavones (5, 7, 10, 12, 14, 20), three flavanones (2, 6, 16), two sterols (3, 8), a fatty acid (1), a phthalate (4), a triterpene (9), and a monoterpene (13). Among them, 14-deoxy-11,12-didehydroandrographolide (17) displayed the most potent preferential cytotoxicity against PANC-1 and PSN-1 cells with PC50 values of 10.0 μM and 9.27 μM, respectively. Microscopical observation, double staining with ethidium bromide (EB) and acridine orange (AO), and flow cytometry with propidium iodide/annexin V double staining indicated that 14-deoxy-11,12-didehydroandrographolide (17) triggered apoptosis-like cell death in NDM with an amino acids and/or serum-sensitive mode.Article · Jul 2015}