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| 1 | Non-Smad pathways in TGF-β signaling显示文摘转变生长因素 -- 尾除了 Smads 利用大量的细胞内部的发信号小径调整细胞的功能的一个宽数组。这些不在经典中, non-Smad 小径被占据 ligand 的受体直接激活到增强,稀释,或不那样调制下游地细胞的回答。这些 non-Smad 小径包括地图 kinase 小径,象 Rho 一样 GTPase 发信号小径,和 phosphatidylinositol-3-kinase/AKT 小径的各种各样的分支。这评论在 non-Smad 小径的分子、生物化学的机制的理解集中于最近的进展。另外,这些 non-Smad 小径的功能也被讨论。 | Ying E Zhang | 2009 | Cell Research2009，19，1： | 67 |
| 2 | PI3K-Akt信号传导通路对糖代谢的调控作用显示文摘磷脂酰肌醇3-激酶(PI3Ks)作为酪氨酸激酶和G蛋白偶联受体的主要下游分子,通过催化产生第二信使3,4,5-三磷酸磷脂酰肌醇(PIP3)并激活Akt、糖原合酶激酶-3(GSK-3)、Forkhead转录因子FoxO1、mTOR(mammalian target of rapamycin)等下游分子,将多种生长因子及细胞因子的信号传递到细胞内,从而对细胞增殖、分化、凋亡和葡萄糖转运等多种生物过程起重要的调节作用.PTEN(phosphatase and tensin homologue)是PI3K信号通路的重要负调节因子.本文将对PI3K-Akt信号通路在糖代谢中的作用予以简要综述. | 迟毓婧 李晶 管又飞 杨吉春 | 2010 | 中国生物化学与分子生物学报2010，26，10： | 78 |
| 3 | 紫草素通过PI3K/Akt通路促进人乳腺癌MCF-7细胞自噬显示文摘目的研究紫草素(Shikonin)对人乳腺癌MCF-7细胞自噬的影响及其作用机制。方法 CCK-8法检测紫草素处理人乳腺癌MCF-7细胞24、48 h细胞的存活率,Western blot方法检测紫草素处理24 h和48 h时LC3、p62、PI3K、Akt、p-PI3K、p-Akt蛋白水平。结果 1μmol.L-1紫草素处理细胞48 h以及2.5、5μmol.L-1紫草素处理MCF-7细胞24 h和48 h时,MCF-7细胞的活力受到明显抑制,LC3-Ⅱ/LC3-Ⅰ值增加,p62表达减少,总PI3K、Akt、p-PI3K、p-Akt均减少。结论紫草素促进乳腺癌MCF-7细胞自噬,其作用机制可能与PI3K/Akt通路受到抑制有关。 | 陈菊英 刘朝纯 曾智 黄文东 杨永飞 朱邦豪 | 2013 | 中国药理学通报2013，29，2： | 51 |
| 4 | Resveratrol provides neuroprotection by regulating the JAK2/STAT3/PI3K/AKT/mTOR pathway after stroke in rats显示文摘Ischemic stroke is a common disease with high mortality and morbidity worldwide.One of the important pathophysiological effects of ischemic stroke is apoptosis.A neuroprotective effect is defined as the inhibition of neuronal apoptosis to rescue or delay the infarction in the surviving ischemic penumbra.Resveratrol is a natural polyphenol that reportedly prevents cerebral ischemia injury by regulating the expression of PI3K/AKT/mTOR.Therefore,this study aimed to elucidate the neuroprotective effect of resveratrol on cerebral ischemia/reperfusion injury and to investigate the signaling pathways and mechanisms through which resveratrol regulates apoptosis in the ischemic penumbra.Rats were subjected to middle cerebral artery occlusion for 2 h followed by 24 h reperfusion.Cerebral infarct volume was measured using 2%TTC staining.TUNEL staining was conducted to evaluate neuronal apoptosis.Western blotting and immunohistochemistry were used to detect the proteins involved in the JAK2/STAT3/PI3K/AKT/mTOR pathway.The results suggested that resveratrol significantly improved neurological function,reduced cerebral infarct volume,decreased neuronal damage,and markedly attenuated neuronal apoptosis;these effects were attenuated by the inhibition of PI3K/AKT with LY294002 and JAK2/STAT3 with AG490.We also found that resveratrol significantly upregulated the expression of p-JAK2,p-STAT3,p-AKT,p-mTOR,and BCL-2 and downregulated expression of cleaved caspase-3 and BAX,which was partially reversed by LY294002 and AG490.These results suggested that resveratrol provides a neuroprotective effect against cerebral ischemia/reperfusion injury,which is partially mediated by the activation of JAK2/STAT3 and PI3K/AKT/mTOR.Resveratrol may indirectly upregulate the PI3K/AKT/mTOR pathway by activating JAK2/STAT3. | Yongying Hou Ke Wang Weijun Wan Yue Cheng Xia Pu Xiufeng Ye | 2018 | Genes & Diseases2018，5，3： | 60 |
| 5 | Panax notogiseng saponin inhibits ischemia-induced apoptosis by activating PI3K/Akt signal pathway in cardiomyocytes显示文摘The panax notoginseng saponin(PNS) had been clinically used for the treatment of cardiovascular diseases and stroke in China.It had been demonstrated that PNS could protect cardiomyocytes from injury induced by ischemi- a,but the underlying molecular mechanisms of this protective effect were still unclear.This study was aimed to investigate the protective effect and molecular mechanisms of PNS on apoptosis in H9c2 cells in vitro and rat myocardial ischemia injury model in vivo.Annexin-V/PI assay shew that PNS could protect H9c2 cells from apoptosis induced by serum, glucose and oxygen deprivation(SGOD) in a dose-dependent manner.However,the anti-apoptotic effect of PNS was reversed by LY294002,a specific PI3K inhibitor.This antiapoptotic effect of PNS was confirmed by JC-1,a specific probe of mitochondrial membrane potential staining.PNS could significantly increase phos-Akt in H9c2 cells by Western blot assays and its effect could be inhibited by LY294002.Furthermore,PNS could improve ischemic-induced left ventricular function as reflected by EF,LVDd and LVDs.PNS could also inhibited cellular apoptosis in myocardial tissues in ischemic rats by TUNEL assay.PNS administration also increased the expression of phos-Akt in rat ischemic myocardial tissues.These results suggested that PNS could protect myocardial cells from apoptosis induced by ischemia in vitro model and in vivo model through activating-PI3K/Akt signal pathway which may be meaningful for further understanding the molecular mechanisms of cardiac protection of PNS.And the results might be useful in treatment of myocardial ischemia in future. | YANG Min,CHEN Shao-Xian,LIU Ju-Li,LIU Xiao-Ying,FU Yong-Heng,ZHANGMeng-zhen,LIN Qiu-Xiong,ZHU Jie-Ning, SHAN Zhi-Xin,YU Xi-yong (Medical Research Center,Guangdong General Hospital, Guangdong Academy of Medical Sciences,Guangzhou 510100,China) | 2011 | 岭南心血管病杂志2011，17，S1： | 47 |
| 6 | 麦冬皂苷B诱导人宫颈癌HeLa细胞自噬的机制显示文摘以人宫颈癌HeLa细胞为研究对象,探讨麦冬皂苷B的抗肿瘤作用及其分子机制。采用MTT检测、流式细胞仪分析、吖啶橙染色、Lyso-Tracker Red染色及HeLa-GFP-LC3转染细胞实验,分别检测HeLa细胞的增殖、凋亡及自噬。结果表明,麦冬皂苷B可抑制细胞增殖,但并不诱导细胞凋亡,可诱导细胞自噬,并引起自噬标志性蛋白Beclin-1表达增加及LC3I转变为LC3II;自噬抑制剂3-MA不但可以抑制该自噬作用而且几乎完全逆转其抗增殖作用,提示其生长抑制作用为自噬依赖性的。Western blotting检测结果表明,麦冬皂苷B抑制AKT、mTOR和p70S6K的磷酸化并上调PTEN,但并不引起Caspase3的活化及PARP的切割。因此,麦冬皂苷B抑制HeLa细胞增殖与凋亡无关,而是通过抑制Akt/mTOR信号通路诱导其发生自噬。 | 许秋菊 侯莉莉 胡国强 谢松强 | 2013 | 药学学报2013，48，6： | 45 |
| 7 | Akt与肿瘤的研究进展显示文摘Akt是细胞生存通路PI3K/Akt的关键分子 ,其持续活化与肿瘤的发生发展密切相关 ,已被定义为癌基因。Akt通过磷酸化mTOR ,P2 1Cip1/WAF1,GSK3,TSC2 ,Foxo家族等多种作用底物 ,促进肿瘤细胞的生长、增殖 ,抑制细胞凋亡 ,促进细胞侵袭和转移 ,促进血管生成 ,抵抗化疗和放疗中细胞的凋亡。Akt可能是肿瘤基因治疗、抗肿瘤药物开发新的作用靶。 | 苗丽君 王静 | 2004 | 国外医学(生理病理科学与临床分册)2004，24，5： | 38 |
| 8 | Sevoflurane postconditioning reduces myocardial reperfusion injury in rat isolated hearts via activation of PI3K/Akt signaling and modulation of Bcl-2 family proteins显示文摘Sevoflurane postconditioning reduces myocardial infarct size.The objective of this study was to examine the role of the phosphatidylinositol-3-kinase(PI3K)/Akt pathway in anesthetic postconditioning and to determine whether PI3K/Akt signaling modulates the expression of pro-and antiapoptotic proteins in sevoflurane postconditioning.Isolated and perfused rat hearts were prepared first,and then randomly assigned to the following groups:Sham-operation(Sham),ischemia/reperfusion(Con),sevoflurane postconditioning(SPC),Sham plus 100 nmol/L wortmannin(Sham+Wort),Con+Wort,SPC+Wort,and Con+dimethylsulphoxide(DMSO).Sevoflurane postconditioning was induced by administration of sevoflurane(2.5%,v/v) for 10 min from the onset of reperfusion.Left ventricular developed pressure(LVDP),left ventricular end-diastolic pressure(LVEDP),maximum increase in rate of LVDP(+dP/dt),maximum decrease in rate of LVDP(?dP/dt),heart rate(HR),and coronary flow(CF) were measured at baseline,R30 min(30 min of reperfusion),R60 min,R90 min,and R120 min.Creatine kinase(CK) and lactate dehydrogenase(LDH) were measured after 5 min and 10 min reperfusion.Infarct size was determined by triphenyltetrazolium chloride staining at the end of reperfusion.Total Akt and phosphorylated Akt(phospho-Akt),Bax,Bcl-2,Bad,and phospho-Bad were determined by Western blot analysis.Analysis of variance(ANOVA) and Student-Newman-Keuls' test were used to investigate the significance of differences between groups.The LVDP,±dP/dt,and CF were higher and LVEDP was lower in the SPC group than in the Con group at all points of reperfusion(P<0.05).The SPC group had significantly reduced CK and LDH release and decreased infarct size compared with the Con group [(22.9±8)% vs.(42.4±9.4)%,respectively;P<0.05].The SPC group also had increased the expression of phospho-Akt,Bcl-2,and phospho-Bad,and decreased the expression of Bax.Wortmannin abolished the cardioprotection of sevoflurane postconditioning.Sevoflurane postconditioning may protect the isolated rat heart.Activation of PI3K and modulation of the expression of pro-and antiapoptotic proteins may play an important role in sevoflurane-induced myocardial protection. | Li-na YU Jing YU Feng-jiang ZHANG Mei-juan YANG Ting-ting DING Jun-kuan WANG Wei HE Tao FANG Gang CHEN Min YAN | 2010 | Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)2010，11，9： | 36 |
| 9 | Resveratrol Induces Apoptosis and Autophagy in T-cell Acute Lymphoblastic Leukemia Cells by Inhibiting Akt/mTOR and Activating p38-MAPK显示文摘Objective To explore the effects of resveratrol-induced apoptosis and autophagy in T-cell acute lymphoblastic leukemia(T-ALL) cells and potential molecular mechanisms. Methods The anti-proliferation effect of resveratrol-induced, apoptosis and autophagy on T-ALL cells were detected by using MTT test, immunofluorescence, electronic microscope, and flow cytometry, respectively. Western blotting was performed for detecting changes of apoptosis-associated proteins, cell cycle regulatory proteins and state of activation of Akt, mTOR, p70S6K, 4E-BP1, and p38-MAPK. Results Resveratrol inhibited the proliferation and induced apoptosis and autophagy in T-ALL cells in a dose and time-dependent manner. It also induced cell cycle arrest at G0/G1 phase via up regulating cyclin-dependent kinase(CDK) inhibitors p21 and p27 and down regulating cyclin A and cyclin D1. Western blotting revealed that resveratrol significantly decreased the expression of antiapoptotic proteins(Mcl-1 and Bcl-2) and increased the expression of proapoptotic proteins(Bax, Bim, and Bad), and induced cleaved-caspase-3 in a time-dependent manner. Significant increase in ratio of LC3-II/LC3-I and Beclin 1 was also detected. Furthermore, resveratrol induced significant dephosphorylation of Akt, mTOR, p70S6K, and 4E-BP1, but enhanced specific phosphorylation of p38-MAPK which could be blocked by SB203580. When autophagy was suppressed by 3-MA, apoptosis in T-ALL cells induced by resveratrol was enhanced.Conclusion Our findings have suggested that resveratrol induces cell cycle arrest,apoptosis,and autophagy in T-ALL cells through inhibiting Akt/mTOR/p70S6K/4E-BP1 and activating p38-MAPK signaling pathways.Autophagy might play a role as a self-defense mechanism in T-ALL cells treated by resveratrol.Therefore,the reasonable inhibition of autophagy in T-ALL cells may serve as a promising strategy for resveratrol induced apoptosis and can be used as adjuvant chemotherapy for T-ALL. | GE Jiao LIU Yan LI Qiang GUO Xia GU Ling MA Zhi Gui ZHU Yi Ping | 2013 | Biomedical and Environmental Sciences2013，26，11： | 38 |
| 10 | 二参三草汤治疗慢性萎缩性胃炎癌前病变的临床观察及其对PTEN、ERK、AKT表达影响的研究显示文摘目的:观察二参三草汤对慢性萎缩性胃炎癌前病变的治疗效果及对PTEN、ERK和AKT表达的影响。方法:40例符合纳入标准的患者随机分为两组,每组20例,治疗组给予二参三草汤,对照组给予胃复春片,疗程均为6个月。观察两组患者临床疗效、内镜、病理疗效及治疗前后PTEN、AKT、ERK表达积分的变化。结果:临床症状缓解总有效率:治疗组95%,对照组65%;内镜下黏膜表现及病理组织学改善情况:治疗组愈显率70%,对照组30%;两组间比较差异显著(P<0.05)。免疫组化结果:治疗组治疗前后PTEN、AKT、ERK的表达差异具有显著统计学意义(P<0.01),而对照组治疗前后AKT、ERK表达水平变化不明显。结论:二参三草汤能明显改善CAG癌前病变的临床症状、内镜下表现及病理组织学表现,其上调抑癌基因PTEN和下调癌基因AKT、ERK的表达可能是二参三草汤治疗慢性萎缩性胃炎癌前病变的部分作用机理。 | 黄婷婷 周晓虹 | 2016 | 中医药信息2016，33，1： | 38 |
| 11 | PI3K/Akt/mTOR自噬通路在人参皂苷Rg1延缓D-gal诱导的卵巢早衰小鼠模型卵巢早衰中的作用显示文摘研究磷脂酰肌醇3-激酶(posphoinositide 3-kinase,PI3K)、蛋白激酶B(protein kinase B,Akt)和哺乳动物雷帕霉素靶蛋白(mammalian target of rapamycin,mTOR)自噬信号通路在人参皂苷Rg_(-1)(ginsenoside Rg_(-1),Rg_(-1))延缓D-半乳糖(D-galactose,D-gal)诱导的卵巢早衰小鼠模型卵巢早衰中的作用。将SPF级雌性BALB/c小鼠54只随机分成PBS组、D-gal组、Rg_(-1)组。D-gal组给予颈背部皮下注射D-半乳糖200 mg·kg^(-1)·d^(-1),连续给药42 d;PBS组给予颈背部注射等时等量磷酸盐缓冲液(PBS),连续注射42 d;Rg_(-1)组在D-gal组处理基础上,于第15天开始给予腹腔注射Rg_(-1)20 mg·kg^(-1)·d^(-1),连续给药28 d,同时D-gal组和PBS组也在第15天开始给予腹腔注射等时等量PBS,连续给药28 d。给药后,检测小鼠动情周期改变,卵巢SA-β-Gal苷酶染色检测卵巢衰老状态改变,Western blot法检测PI3K,Akt,mTOR,S6k,LC3-Ⅱ,P16^(INK4a)蛋白表达的改变。荧光定量PCR法检测衰老调控因子PI3K,Akt,mTOR,S6k,P16^(INK4a)mRNA表达的改变。研究结果显示,与PBS组比较,D-gal组第3周开始出现动情周期紊乱,卵巢SA-β-半乳糖苷酶染色阳性率升高,衰老标记物P16^(INK4a)表达量升高,自噬信号分子LC3-Ⅱ表达量降低;Rg_(-1)作用后,Rg_(-1)组卵巢SA-β-半乳糖苷酶染色阳性率降低,衰老标记物P16^(INK4a)表达量低于D-gal组,自噬信号分子LC3-Ⅱ表达量高于D-gal组。与PBS组比较,D-gal组PI3K,Akt,mTOR,S6k蛋白和mRNA表达上调,Rg_(-1)组Akt,mTOR,S6k蛋白表达上调,PI3K,mTOR mRNA表达上调。Rg_(-1)作用后,Rg_(-1)组PI3K,Akt,mTOR,S6k蛋白表达量低于D-gal组,Akt,mTOR,S6k mRNA表达量低于D-gal组。研究结果提示,Rg_(-1)具有延缓D-gal诱导的卵巢早衰小鼠模型中卵巢早衰的作用,PI3K/Akt/mTOR自噬信号通路在其中发挥重要功能。 | 刘小虎 赵志慧 周玥 王翠丽 韩艳军 周雯 | 2020 | 中国中药杂志2020，45，24： | 36 |
| 12 | PI3K/Akt信号通路在骨质疏松病理过程中的作用显示文摘磷脂酰肌醇三激酶/蛋白激酶B(PI3K/Akt)信号通路是调节细胞增殖、分化、存活、迁移和代谢过程的最为重要的一个信号通路。越来越多的证据表明,骨组织中的许多信号分子能够选择性激活PI3K/Akt信号通路的相关基因,通过调控成骨细胞和破骨细胞的活动,破坏骨重建过程中骨形成与骨吸收的动态平衡,在骨质疏松的发生和发展中扮演着非常重要的角色。 | 陈亚辉 龚忠勤 崔燎 | 2015 | 中国骨质疏松杂志2015，21，3： | 32 |
| 13 | PI3K/Akt/mTOR信号转导途径与非小细胞肺癌的关系显示文摘背景与目的PI3K/Akt/mTOR通路失调对肺癌形成可能具有重要作用,本研究通过分析非小细胞肺癌组织中PI3K/Akt/mTOR信号转导途径中VEGF、PI3K、Akt、mTOR基因的表达水平,探讨PI3K/Akt/mTOR信号转导途径与非小细胞肺癌之间的关系。方法外科手术中获取40例非小细胞肺癌组织及30例癌旁组织,应用逆转录聚合酶链反应(reverse transcriptase polymerase chain reaction,RT-PCR)技术检测癌及癌旁组织中VEGF、PI3K、Akt、mTOR基因的表达水平。结果非小细胞肺癌组织中VEGF、PI3K、Akt、mTOR基因的表达水平分别为(40±59)%、(61±23)%、(77±32)%、(43±21)%,癌旁组织中VEGF、PI3K、Akt、mTOR基因的表达水平分别为(16±40)%、(23±16)%、(10±12)%、(20±17)%,非小细胞肺癌组织中VEGF、PI3K、Akt、mTOR基因的表达水平均高于癌旁组织(P<0.01)。联合应用4个基因表达作为NSCLC诊断标志,诊断的敏感性达到87.5%,特异性为90%。结论非小细胞肺癌中PI3K/Akt/mTOR信号转导途径相关基因表达水平明显上调,说明该通路在非小细胞肺癌中被激活。联合检测VEGF、PI3K、Akt、mTOR的表达水平改变可能作为NSCLC的诊断标志。 | 岳文涛 王小敏 王玥 | 2009 | 中国肺癌杂志2009，12，4： | 29 |
| 14 | PI3K/Akt信号通路与肝纤维化显示文摘PI3K/AKT信号通路可以通过调控基因表达,从而在细胞的存活、分化、生长、运动和凋亡等多种生理和病理过程中起到重要作用。尤其在肝纤维化的进展中,此信号通路发挥了重要的调节作用。本文将对目前有关PI3K/AKT信号通路在参与肝纤维化形成中,如何调控细胞外基质的降解、影响HSC的活化及调节肝窦毛细血管化等作用机制作一综述。这些资料不仅可以揭示相关疾病条件下,多个细胞与信号因子之间复杂的相互作用机制,而且能够突出通过阻断PI3K/AKT信号通路可以保护和治疗肝纤维化这一潜在的临床意义。 | 潘澎 刘绍能 | 2013 | 临床肝胆病杂志2013，29，5： | 29 |
| 15 | 槲皮素对非酒精性脂肪性肝炎大鼠的影响显示文摘目的探讨槲皮素对非酒精性脂肪性肝炎大鼠的影响。方法 36 只大鼠给予高脂饲料 10 周造模后,随机分为空白组、模型组及槲皮素低、高剂量组(40、 80mg/kg),每组9只。 HE、油红O、 Masson染色检测大鼠肝组织炎症损伤、脂肪变性,纤维化程度,免疫组化F4/80检测Kupffer细胞活化水平, Western blot检测大鼠肝脏PI3K、 AKT、NF κB p65、 p AKT1、 p NF κB p65 蛋白表达,荧光定量 PCR 检测大鼠肝脏 PI3 K、 AKT1 、 AKT2 、 NF κB mRNA 表达。结果与模型组比较,槲皮素高剂量组明显改善大鼠肝脏脂质沉积和肝脏纤维化,减轻炎症细胞浸润,降低 NAS 评分,减少Kupffer细胞活化水平(P<0 05);还能显著提高PI3K、 AKT表达,降低NF κB表达(P<0 05)。结论槲皮素能通过调控PI3K/AKT/NF κB信号通路来改善非酒精性脂肪性肝炎大鼠肝组织脂肪变性程度,减轻肝脏炎症。 | 刘鸣昊 张丽慧 马庆亮 赵文霞 | 2019 | 中成药2019，41，8： | 29 |
| 16 | Roles of the MEK1/2 and AKT pathways in CXCL12/CXCR4 induced cholangiocarcinoma cell invasion显示文摘AIM:To evaluate the expression of C-X-C motif chemokine receptor 4(CXCR4)and its signaling cascades,which were previously identified as a key factor for cancer cell progression and metastasis,in cholangiocarcinoma cell lines.METHODS:The expression of CXCR4 and its signaling cascades were determined in the cholangiocarcinoma cell lines(RMCCA1 and KKU100)by Western blotting.The invasion assays and the detection of actin polymerization were tested in these cholangiocarcinoma cells treated with CXC chemokine ligand-12(CXCL12).RESULTS:Expression of CXCR4 was detected in both cholangiocarcinoma cell lines and activation of CXCR4 with CXCL12 triggered the signaling via the extracellular signal-regulated kinase-1/2(ERK1/2)and phosphoinositide 3-kinase(PI3K)and induction of cholangiocarcinoma cell invasion,and displayed high levels of actin polymerization.Addition of CXCR4 inhibitor(AMD3100)abrogated CXCL12-induced phosphorylation of MEK1/2 and Akt in these cells.Moreover,treatment with MEK1/2 inhibitor(U0126)or PI3K inhibitor(LY294 002)also attenuated the effect of CXCL12-induced cholangiocarcinoma cell invasion.CONCLUSION:These results indicated that the activation of CXCR4 and its signaling pathways(MEK1/2 and Akt)are essential for CXCL12-induced cholangiocarcinoma cell invasion.This rises Implications on a potential role for the inhibition of CXCR4 or its signal cascades in the treatment of cholangiocarcinoma. | Kawin Leelawat Surang Leelawat Siriluck Narong Suradej Hongeng | 2007 | World Journal of Gastroenterology2007，13，10： | 27 |
| 17 | PTEN-PI3K/AKT细胞信号转导通路与肿瘤显示文摘PTEN基因是近年来发现的一种新的肿瘤抑制基因,其产物PTEN蛋白具有脂质磷酸酶活性和蛋白磷酸酶活性。PI3K/AKT信号通路为生物体内重要的生存信号通路。实验证实PTEN主要是通过其脂质磷酸酶活性作用于PI3K的下游靶分子PIP3从而阻断PI3K/AKT信号通路来实现其抑癌作用,故有学者将它们称为PTEN-PI3K/AKT信号转导通路。本文中从细胞凋亡、细胞周期调节、细胞迁移与侵袭、血管形成、肿瘤耐药、肿瘤免疫逃逸等多个角度综述了PTEN-PI3K/AKT信号转导通路与肿瘤的关系。 | 陈培 张钦宪 | 2010 | 癌变.畸变.突变2010，22，6： | 28 |
| 18 | P13K and Akt as molecular targets for cancer therapy: current clinical outcomes显示文摘 | Ipsita PAL, Mahitosh MANDAq | 2012 | Acta Pharmacologica Sinica2012，33，12： | 28 |
| 19 | 葛根素对链脲佐菌素诱导的糖尿病小鼠降糖作用显示文摘目的:探讨葛根素(puerarin,Pue)对链脲佐菌素(STZ)诱导糖尿病模型小鼠的降糖作用。方法:C57BL/6J小鼠以一次性注射STZ150 mg·kg-1建立糖尿病小鼠模型;动物包括正常对照组(con)、模型组(STZ)、葛根素组(Pue)(100 mg·kg-1),其中Pue组灌胃给药,模型组及对照组给予0.2%CMC-Na,每日1次,4周后检测小鼠空腹血糖(FBG)、空腹血浆胰岛素(FINS)和口服糖耐量(OGTT);显微镜观察HE染色及免疫荧光染色胰腺组织形态学的改变;Western Blot检测肝脏组织中p-AKT,p-GSK-3β蛋白水平;实时荧光定量PCR(RT-PCR)检测UCP2 mRNA表达变化。结果:与模型组比较,葛根素组小鼠的FBG明显降低,FINS含量升高,OGTT有所改善;模型组胰岛形态结构被破坏,而葛根素组有明显改善,β细胞数目增加,并且肝脏中p-AKT和p-GSK-3β水平上调,而UCP2 mRNA表达降低。结论:本研究表明葛根素的降糖作用机制可能与保护胰岛β细胞,改善肝脏功能,调控UCP2 mRNA水平,激活胰岛素受体下游AKT通路激活相关。 | 杨蕾 舒娈 姚冬冬 贾晓斌 余嗣明 | 2014 | 中国医院药学杂志2014，34，16： | 28 |
| 20 | The PI3K/Akt/m TOR pathway in ovarian cancer: therapeutic opportunities and challenges显示文摘The phosphatidylinositol 3 kinase(PI3K) pathway is frequently altered in cancer, including ovarian cancer(OC). Unfortunately, despite a sound biological rationale and encouraging activity in preclinical models, trials of first-generation inhibitors of mammalian target of rapamycin(m TOR) in OC have demonstrated negative results. The lack of patient selection as well as resistance to selective m TOR complex-1(m TORC1) inhibitors could explain the disappointing results thus far. Nonetheless, a number of novel agents are being investigated, including dual m TORC1/m TORC2, Akt, and PI3 K inhibitors. Although it is likely that inhibition of the PI3K/Akt/m TOR pathway may have little effect in unselected OC patients, certain histological types, such as clear cell or endometrioid OC with frequent phosphatidylinositol-4,5-biphosphate 3-kinase, catalytic subunit alpha(PIK3CA) and/or phosphatase and tensin homolog(PTEN) alterations, may be particularly suited to this approach. Given the complexity and redundancy of the PI3 K signaling network, PI3 K pathway inhibition may be most useful in combination with either chemotherapy or other targeted therapies, such as MEK inhibitors, anti-angiogenic therapy, and hormonal therapy, in appropriately selected OC patients. Here, we discuss the relevance of the PI3 K pathway in OC and provide an up-to-date review of clinical trials of novel PI3 K inhibitors alone or in combination with cytotoxics and novel therapies in OC. In addition, the challenges of drug resistance and predictive biomarkers are addressed. | Bianca Cheaib Aurélie Auguste Alexandra Leary | 2015 | Chinese Journal of Cancer2015，34，1： | 27 |
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