摘要：
Background: Warfarin is the most extensively used coumarin anticoagulant. It has been shown that the anticoagulant effect of warfarin is associated with genetic variation. Apolipoprotein E (ApoE) is a possible candidate to influence the maintenance dose of warfarin. ApoE affects the vitamin K cycle by mediating the uptake of vitamin K into the liver. The vitamin K cycle is the drug target of warfarin. However, the association between genetic variants of the APOE gene and warfarin dose requirement is still controversial. Methods: Revman 5.3 software was used to analyze the relationship between APOE genotypes and warfarin dose requirements. Results: In our meta-analysis, the E2/E2 genotype was significantly associated with warfarin dose. E2/E2 patients required 12% (P=0.0002) lower mean daily warfarin dose than E3/E3 carriers. In addition, subgroup analysis showed that Asians with the E4/E4 genotype tended to need lower warfarin maintenance doses, while the African- Americans E4/E4 carriers needed slightly higher doses than E3/E3 carriers, however these subgroups were very small. Conclusion: This is the first meta-analysis of the association between APOE genotypes and warfarin dose. APOE E2/E2 might be one of the factors affecting warfarin dose requirements. The effect of APOE may vary between ethnicities. This article is protected by copyright. All rights reserved.
摘要：
Minimally modified low-density lipoprotein (mmLDL) is a well-known risk factor for cardiovascular diseases. The present study was designed to investigate the role of mmLDL in the endothelium-dependent relaxation of mouse mesenteric arteries. A sensitive myograph system was employed to examine the endothelial function of mesenteric arteries. mRNA and protein expression levels were determined using real-time PCR and Western blotting, respectively. The ultra-microstructure of mesenteric vascular beds was investigated using a transmission electron microscope. The results showed that mmLDL significantly impaired the acetylcholine-induced (3 x 10(-10) to 1 x 10(-4) M) endothelium-dependent relaxation of mouse mesenteric arteries with markedly reduced plC(50) (p < 0.05) and R-max values (p < 0.001). In addition, mmLDL increased the levels of superoxide production and nitrotyrosine concentration and impaired the endothelial microstructure with decreased K(ca)3.1 and K(ca)2.3 expression. In conclusion, mmLDL increases superoxide and nitro-tyrosine levels, damages endothelial microstructure with decreased K(ca)3.1 and K(ca)2.3 expression, and ultimately attenuates relaxation mediated by nitric oxide- and endothelium-derived hyperpolarizing factor. (C) 2016 S. Karger AG, Basel
摘要：
LXR α could have the anti-proliferative effect on multiple cancer cells including breast cancer. However, the mechanisms of LXR α regulating the breast cancer cells remain unclear. This study is to investigate the different expression of LXR α, NF-κB p65 and cyclinD1 in the proliferation of human breast cancer cells. At first, LXR α, NF-κB p65 and cyclinD1 expression were detected by immunohistochemical staining in human breast cancer and paired adjacent breast tissues (n=60). As a result, the three kinds of protein were mainly expressed in cell nuclei. Among them, NF-κB p65 and cyclinD1 were higher expressed in breast cancer tissues than in adjacent tissues while LXR α was lower expressed. Then, MTT assay was used to detect the proliferation of MCF-7 cells and Western blot was used to examine the expression of the three kinds of protein. TO901317 (a kind of artificial agonists against LXRs especially for LXR α) could increase LXR α expression, but decrease NF-κB p65 and cyclinD1 expression and suppress the proliferation of MCF-7 cells in a dose-and time-dependent manner (P< 0.05). Finally, the effects of LXR α siRNA and pyrrolidinedithiocarbamic acid (PDTC, an inhibitory of NF-κB) on TO901317 were observed respectively. LXR α siRNA could significantly decrease the up-regulation of LXR α expression and reverse the inhibited effect of TO901317 on cyclinD1 and NF-κB p65 expression and MCF-7 cell proliferation(P < 0.05) while PDTC could strengthen the inhibition of cell proliferation and further down-regulate NF-κB p65 and cyclinD1 expression induced by TO901317 (P< 0.05), but have little effect on LXR α. In a conclusion, the expression of LXR α, NF-κB p65 and cyclinD1 plays an important role in the proliferation of human breast cancer cells, so as to provide a new method for the molecular targeting treatment of breast cancer in the future.
摘要：
UNLABELLED: Syphilis is a multistage sexually transmitted disease that remains a serious public health concern worldwide. The coexistence of Treponema pallidum with other closely related members of spirochaeta, such as Leptospira spp. and Borrelia burgdorferi, has complicated the serodiagnosis due to cross-reactive antigens. In this study, recombinant Tp0821 protein was expressed in Escherichia coli and purified by metal affinity chromatography. Then enzyme-linked immunosorbent assays (ELISAs) based on Tp0821 for the detection of specific antibodies were established. The relative positive rates of the IgM ELISA and the IgG ELISA were found to be 91.0 and 98.3%, respectively, when screening 578 syphilis specimens. The specificities were 94.3 and 100%, respectively, when cross-checking with serum samples obtained from 30 patients with Lyme disease, five patients with leptospirosis, and 52 uninfected controls. In addition, relative positive rates and specificities of Tp0821 for human sera were all 100% in Western blotting. When compared to the syphilis diagnostic tests commonly used in clinical settings, we found that the results of Tp0821-based ELISAs correlated well with the results of the treponemal tests, specifically the T. pallidum particle agglutination (TP-PA) test and the chemiluminescent immunoassay (CIA). Thus, these findings identify Tp0821 as a novel serodiagnostic candidate for syphilis. SIGNIFICANCE AND IMPACT OF THE STUDY: In this study, we expressed and purified the Treponema pallidum protein Tp0821 and developed Tp0821-based enzyme-linked immunosorbent assays (ELISAs) for the detection of specific antibodies. The serodiagnostic performance of the recombinant protein was then evaluated. When compared to the results of syphilis diagnostic tests commonly used in clinical settings, we found that the reactivities of syphilitic sera with the recombinant antigen correlated well with the results of the treponemal tests, specifically the T. pallidum particle agglutination (TP-PA) test and the chemiluminescent immunoassay (CIA). Thus, the recombinant protein shows promise as a new diagnostic antigen in the ELISAs.
通讯机构：
[Li, Lanfang] U;Univ South China, Hunan Prov Cooperat Innovat Ctr Mol Target New Dr, Inst Pharm & Pharmacol, Learning Key Lab Pharmacoprote, Hengyang 421001, Peoples R China.
摘要：
The G protein-coupled receptor APJ elicits cellular response to diverse extracellular stimulus. Accumulating evidence reveals that APJ receptor plays a prominent role in the cardiomyocyte adapting to hypertrophic stimulation. At present, it remains obscure that the regulatory mechanism of APJ receptor in myocardial hypertrophy. The natural endogenous ligands apelin and Elabela as well as agonists maintain high affinity for the APJ receptor and drive its internalization. Ligand-activated receptor internalization is mainly performed by clathrin-mediated endocytic pathway. Simultaneously, clathrin-mediated endocytosis takes participate in the occurrence and development of cardiac hypertrophy. In this study, we hypothesize that natural ligands and agonists induce the mechanosensitive APJ internalization via clathrin-mediated endocytosis. APJ internalization may contribute to the development of cardiac hypertrophy. The mechanosensitive APJ internalization via clathrin-mediated endocytosis may be a new molecular mechanism of cardiac hypertrophy. (C) 2016 Elsevier Ltd. All rights reserved.
摘要：
In human cells, ribonuclease (RNase) H2 complex is the predominant source of RNase H activities with possible roles in nucleic acid metabolism to preserve genome stability and to prevent immune activation. Dysfunction mutations in any of the three subunits of human RNase H2 complex can result in embryonic/perinatal lethality or cause Aicardi-Goutieres syndrome (AGS). Most recently, increasing findings have shown that human RNase H2 proteins play roles beyond the RNase H2 enzymatic activities in health and disease. Firstly, the biochemical and structural properties of human RNase H2 proteins allow their interactions with various partner proteins that may support functions other than RNase H2 enzymatic activities. Secondly, the disparities of clinical presentations of AGS with different AGS-mutations and the biochemical and structural analysis of AGS-mutations, especially the results from both AGS-knockin and RNase H2-null mouse models, suggest that human RNase H2 complex has certain cellular functions beyond the RNase H2 enzymatic activities to prevent the innate-immune-mediated inflammation. Thirdly, the subunit proteins RNASEH2A and RNASEH2B respectively, not related to the RNase H2 enzymatic activities, have been shown to play a certain role in the pathophysiological processes of different cancer types. In this minireview, we aims to provide a brief overview of the most recent investigations into the biological functions of human RNase H2 proteins and the underlying mechanisms of their actions, emphasizing on the new insights into the roles of human RNase H2 proteins playing beyond the RNase H2 enzymatic activities in health and disease. (C) 2015 Elsevier Ltd. All rights reserved.
摘要：
DBU-promoted trifluoromethylation of aryl iodides with difluoromethyltriphenylphosphonium bromide (DFPB) in the presence of copper source is described. In this transformation, DBU not only acts as base to deprotonate the difluoromethyl group in DFPB to generate difluoromethylene phosphonium ylide Ph_3P~+CF_2~-,but also converts the difluorocarbene generated from ylide Ph_3P~+CF_2~-- into trifluoromethyl anion, finally resulting in the trifluoromethylation of aryl iodides. The reactions proceeded smoothly to afford expected products in moderate to good yields.
摘要：
Heterogeneous nuclear ribonucleoprotein K (hnRNP K) is one of the major pre-mRNA-binding proteins, that is involved in translational modifications. In our previous studies, we found that hnRNP K is associated with human gastric cancer. The protein levels of hnRNP K were detected in cell lines and tissue microarrays. The correlation between hnRNP K expression and patient survival rate was evaluated by Kaplan-Meier survival analysis. In addition, we also detected hnRNP K expression in preoperative and postoperative serum samples from patients with gastric cancer, and serum samples from healthy volunteers. We found that hnRNP K was overexpressed in the gastric cancer cell lines. The levels of hnRNP K were significantly elevated in the gastric cancer tissues compared with that noted in the tumor-adjacent gastric mucosal and normal gastric mucosal sampes, and hnRNP K expression was found to correlate with tumor stage and lymph node metastasis. However, the level of serum hnRNP K did not differ significantly between gastric cancer patients and healthy volunteers. We also found that patients whose tumors showed elevated expression of hnRNP K had poor survival. The present study suggests that hnRNP K is a promising tissue biomarker for diagnosing gastric cancer and is a prognostic indicator for patients with gastric cancer.
通讯机构：
[Tang, Shengsong] H;[Tang, Shengsong] U;Hunan Univ Med, Biomed Res Ctr, Huaihua 418000, Peoples R China.;Univ South China, Inst Pharm & Pharmacol, Dept Histol & Embryol, Hengyang 421001, Peoples R China.
关键词：
Macrophage colony-stimulating factor;chemoresistance;apoptosis;autophagy;breast cancer
摘要：
Macrophage colony-stimulating factor is a vital factor in maintaining the biological function of monocyte–macrophage lineage. It is expressed in many tumor tissues and cancer cells. Recent findings indicate that macrophage colony-stimulating factor might contribute to chemoresistance, but the precise mechanisms are unclear. This study was to explore the effect of macrophage colony-stimulating factor on doxorubicin resistance in MCF-7 breast cancer cells and the possible mechanism. In the study, the human breast cancer cells, MCF-7, were transfected with macrophage colony-stimulating factor. We document that cytoplasmic macrophage colony-stimulating factor induces doxorubicin resistance and inhibits apoptosis in MCF-7 cells. Further studies demonstrated that cytoplasmic macrophage colony-stimulating factor-mediated apoptosis inhibition was dependent on the activation of PI3K/Akt/Survivin pathway. More importantly, we found that macrophage colony-stimulating factor-induced autophagic cell death in doxorubicin-treated MCF-7 cells. Taken together, we show for the first time that macrophage colony-stimulating factor-induced doxorubicin resistance is associated with the changes in cell death response with defective apoptosis and promotion of autophagic cell death.
作者机构：
[Jiang, H; Su, Q; Zhang, Shuo; Su, Bo; Su, Qi; Zhou, Zhi-Gang; Ling, Hui; Jiang, Hao; Ai, Xiao-Hong; Su, Jian; Yang, Bang-Min; Zeng, Ying; Wu, You-Hua; Xia, Hong; Zeng, Xi; Liu, Fang; Ma, Yan-Hua] Univ South China, Affiliated Hosp 1, Ctr Gastr Canc Res Hunan Prov, Hengyang 421001, Hunan, Peoples R China.;[Zhang, Shuo; Su, Bo; Su, Qi; Zhou, Zhi-Gang; Ling, Hui; Su, Jian; Yang, Bang-Min; Zeng, Ying; Xia, Hong; Zeng, Xi; Liu, Fang; Ma, Yan-Hua] Univ South China, Key Lab Canc Cellular & Mol Pathol Hunan Prov Uni, Canc Res Inst, Hengyang 421001, Hunan, Peoples R China.;[Su, Bo] Univ South China, Inst Pharm & Pharmacol, Key Lab Pharmacoprote Hunan Prov Univ, Hengyang 421001, Hunan, Peoples R China.;[Su, Jian] Univ South China, Affiliated Hosp 2, Dept Pathol, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Jiang, H; Su, Q; Su, Qi] U;Univ South China, Affiliated Hosp 1, Ctr Gastr Canc Res Hunan Prov, Hengyang 421001, Hunan, Peoples R China.;Univ South China, Key Lab Canc Cellular & Mol Pathol Hunan Prov Uni, Canc Res Inst, Hengyang 421001, Hunan, Peoples R China.
关键词：
LIMK1;diallyl disulfide;gastric cancer cell epithelial-mesenchymal transition;invasion;proliferation
摘要：
Diallyl disulfide (DADS) has been shown to have multi-targeted antitumor activities. We have previously discovered that it has a repressive effect on LIM kinase-1 (LIMK1) expression in gastric cancer MGC803 cells. This suggests that DADS may inhibit epithelial-mesenchymal transition (EMT) by downregulating LIMK1, resulting in the inhibition of invasion and growth in gastric cancer. In this study, we reveal that LIMK1 expression is correlated with tumor differentiation, invasion depth, clinical stage, lymph node metastasis, and poor prognosis. DADS downregulated the Rac1-Pak1/Rock1-LIMK1 pathway in MGC803 cells, as shown by decreased p-LIMK1 and p-cofilin1 levels, and suppressed cell migration and invasion. Knockdown and overexpression experiments performed in vitro demonstrated that downregulating LIMK1 with DADS resulted in restrained EMT that was coupled with decreased matrix metalloproteinase-9 (MMP-9) and increased tissue inhibitor of metalloproteinase-3 (TIMP-3) expression. In in vitro and in vivo experiments, the DADS-induced suppression of cell proliferation was enhanced and antagonized by the knockdown and overexpression of LIMK1, respectively. Similar results were observed for DADS-induced changes in the expression of vimentin, CD34, Ki-67, and E-cadherin in xenografted tumors. These results indicate that downregulation of LIMK1 by DADS could explain the inhibition of EMT, invasion and proliferation in gastric cancer cells.
作者机构：
[Liu, Jie; He, Ruo-Hui; Zhou, Hong-Hao; Tang, Yong-Jun; He, Yi-Jing] Cent S Univ, Xiangya Hosp, Dept Clin Pharmacol, Changsha 410008, Hunan, Peoples R China.;[Liu, Jie; He, Ruo-Hui; Zhou, Hong-Hao; Tang, Yong-Jun; He, Yi-Jing] Cent S Univ, Hunan Key Lab Pharmacogenet, Inst Clin Pharmacol, Changsha 410078, Hunan, Peoples R China.;[Liu, Jie; He, Ruo-Hui; Zhou, Hong-Hao; Tang, Yong-Jun; He, Yi-Jing] Univ South China, Cooperat Innovat Ctr Mol Target New Drug Study, Hengyang 421001, Hunan, Peoples R China.;[McLeod, Howard L.] H Lee Moffitt Canc Ctr & Res Inst, Div Populat Sci, DeBartolo Family Personalized Med Inst, Tampa, FL 33612 USA.
通讯机构：
[Liu, Jie] C;Cent S Univ, Xiangya Hosp, Dept Clin Pharmacol, Changsha 410008, Hunan, Peoples R China.
关键词：
cancer progression;polymorphisms;tumor biology behaviors;beta-adrenergic receptors;beta-blockers
摘要：
β-ARs are extensively spread in different tissues of our body, which could be activated by neurotransmitters norepinephrine and epinephrine to mediate physiological function and abnormal states including cancer. Recently, β-AR blockers could have significant implications in cancer therapy. But the precise molecular mechanisms are far from being fully understood. Through identifying the β-AR system signal pathways relevant to cancer, we can understand the mechanisms of β-blockers used for cancer treatment. What's more, retrospective clinical data made β-blockers jump out of the traditional field of cardiovascular disease and strengthened our confidence in cancer therapy. At last, genetic studies of β-adrenergic system offered crucial genes to analyze the effects of polymorphisms on cancer susceptibility, therapy response and prognosis of cancer patients.
摘要：
The development of slow release nano-sized carriers for efficient antineoplastic drug delivery with a biocompatible and biodegradable pectin-based macromolecular pro-drug for tumor therapy has been reported in this study. Pectin-doxorubicin conjugates (PDC), a macromolecular pro-drug, were prepared via an amide condensation reaction, and a novel amphiphilic core-shell micell based on a PDC macromolecular pro-drug (PDC-M) was self-assembled in situ, with pectin as the hydrophilic shell and doxorubicin (DOX) as the hydrophobic core. Then the chemical structure of the PDC macromolecular pro-drug was identified by both Fourier transform infrared spectroscopy (FTIR) and nuclear magnetic resonance spectroscopy (1H-NMR), and proved that doxorubicin combined well with the pectin and formed macromolecular pro-drug. The PDC-M were observed to have an unregularly spherical shape and were uniform in size by scanning electron microscopy (SEM). The average particle size of PDC-M, further measured by a Zetasizer nanoparticle analyzer (Nano ZS, Malvern Instruments), was about 140 nm. The encapsulation efficiency and drug loading were 57.82% ± 3.7% (n = 3) and 23.852% ±2.3% (n = 3), respectively. The in vitro drug release behaviors of the resulting PDC-M were studied in a simulated tumor environment (pH 5.0), blood (pH 7.4) and a lysosome media (pH 6.8), and showed a prolonged slow release profile. Assays for antiproliferative effects and flow cytometry of the resulting PDC-M in HepG2 cell lines demonstrated greater properties of delayed and slow release as compared to free DOX. A cell viability study against endothelial cells further revealed that the resulting PDC-M possesses excellent cell compatibilities and low cytotoxicities in comparison with that of the free DOX. Hemolysis activity was investigated in rabbits, and the results also demonstrated that the PDC-M has greater compatibility in comparison with free DOX. This shows that the resulting PDC-M can ameliorate the hydrophobicity of free DOX. This work proposes a novel strategy for in-situ one-step synthesis of macromolecular pro-drugs and fabrication of a core-shell micelle, demonstrating great potential for cancer chemotherapy.
摘要：
Self-assembled peptide nanomaterials display the advantageous properties of injectability, biodegradability and biocompatibility. These peptide nanomaterials, by self-assembling, can be widely applied in such fields as drug delivery (small molecules and large molecules), regenerative medicine and nanobiotechnology. In this review, we mainly discuss the properties of these peptide nanomaterials in their physical, chemical and biological aspects. Also discussed are recent advances in their potential applications as drug delivery systems and for uses in regenerative medicine. These current advances show a bright future for the development and clinical applications of self-assembled peptide-based nanotechnology and nanomedicine. However, there are still some big challenges for us to face before these peptide nanomaterials eventually can be used for the treatment of human diseases.
期刊：
NITRIC OXIDE-BIOLOGY AND CHEMISTRY,2016年60:59-68 ISSN：1089-8603
通讯作者：
Chen, Xiao-Ping;Zhang, Zan-Lin
作者机构：
[Zeng, Wen-Jing; Kuang, Da-Bin; Zhou, Ji-Peng; Yu, Lin-Yu; Chen, Xiao-Ping] Cent South Univ, Xiangya Hosp, Dept Clin Pharmacol, Changsha 410008, Hunan, Peoples R China.;[Zeng, Wen-Jing; Kuang, Da-Bin; Zhou, Ji-Peng; Yu, Lin-Yu; Chen, Xiao-Ping] Cent South Univ, Inst Clin Pharmacol, Hunan Key Lab Pharmacogenet, Changsha 410078, Hunan, Peoples R China.;[Zeng, Wen-Jing; Kuang, Da-Bin; Chen, Xiao-Ping] Univ South China, Cooperat Innovat Ctr Mol Target New Drug Study, Hengyang 421001, Hunan, Peoples R China.;[Zhou, Ji-Peng] Cent South Univ, Xiangya Hosp, Dept Cardiovasc Med, Changsha 410008, Hunan, Peoples R China.;[Zhang, Zan-Lin; Xiao, Jian] Cent South Univ, Xiangya Hosp, Dept Pharm, Changsha 410008, Hunan, Peoples R China.
通讯机构：
[Chen, Xiao-Ping; Zhang, Zan-Lin] C;Cent South Univ, Xiangya Hosp, Dept Clin Pharmacol, Changsha 410008, Hunan, Peoples R China.;Cent South Univ, Xiangya Hosp, Dept Pharm, Changsha 410008, Hunan, Peoples R China.
关键词：
DDAH1;miR-21;microRNA sponge
摘要：
Objective: To investigate whether microRNA (miRNA) miR-21 regulates dimethylarginine dimethylaminohydrolase 1 (DDAH1) expression through binding 3'-UTR region directly in human umbilical venous endothelial cells (HUVECs) and to explore whether DDAH1-V2/V3 transcripts can function as microRNA sponge, thereby modulating DDAH1-V1 expression. Methods: The DDAH1 3'-UTR containing miR-21 recognizing sequence was cloned into PmirGLO dualluciferase miRNA target expression plasmid to construct PmirGLO-miR-21. The plasmid and miR-21 (at concentrations of 25, 50, 100 nM, respectively) or negative control (100 nM) were co-transfected into HUVECs, luciferase activity was detected at 24 h. HUVECs were incubated with 2 mu g/ml Actinomycin D for the indicated time after miR-21 (25 nM) transfection, half-lives of DDAH1 mRNA were determined. HUVECs were transfected with PmirGLO-miR-21 alone or co-transfected with miR-21 for 24 h, DDAH1 transcripts mRNA, eNOS activity and DDAH1 protein expression were determined. Results: MiR-21 decreased luciferase activity of PmirGLO-miR-21 in a dose-dependent manner (P < 0.05 for 25 nM miR-21, P < 0.01 for 50 nM and 100 nM miR-21), and miR-21 inhibitor increased reporter activity of PmirGLO-miR-21 and mRNA expression of all three DDAH1 transcript variants significantly (P < 0.05, respectively). The degree of increase in endogenous DDAH1 mRNA expression by miR-21 inhibitor was more obvious for DDAH1-V3. Overexpression of miR-21 decreased mRNA expression and mRNA half-life time of all DDAH1 transcripts significantly (P < 0.05), and DDAH1-V2 displayed significantly decreased half-life time than DDAH1-V1 and -V3 with or without miR-21 transfection (P < 0.05, respectively). MiR-21 (100 nM) decreased DDAH1 protein expression and eNOS activity significantly (P < 0.05), which was reversed by PmirGLO-miR-21 transfection (P < 0.05). Transfection of PmirGLO-miR-21 alone increased intracellular miR-21 expression by approximately 5.6-fold, but only showed a trend of increase in DDAH1 protein expression. Conclusion: Our results confirmed DDAH1 3'-UTR as a target for miR-21, and endogenous miR-21 showed increased inhibitory effect on DDAH1-V3 transcript. DDAH1 3'-UTR, especially for DDAH1-V3, may function as miR-21 sponge to regulate DDAH1 protein expression. Modulation of miR-21-DDAH1 interaction may provide a new approach for tackling cardiovascular diseases. (C) 2016 Elsevier Inc. All rights reserved.
期刊：
Journal of Pharmacy and Pharmacology,2016年68(6):751-761 ISSN：0022-3573
通讯作者：
Tang Guotao
作者机构：
[Huang Rongbin] First Peoples Hosp Xiangtan City, Xiangtan, Peoples R China.;[Deng Xiangping; Xiang Lei; Cao Xuan; Li Lanfang; Tang Guotao; Liu Ying; Yu Cuiyun] Univ South China, Learning Key Lab Pharmacoprote, Inst Pharm & Pharmacol, Hengyang 421001, Hunan, Peoples R China.;[Chen Yanming] Mu Dan Jiang You Bo Pharmacert Co Ltd, Mudanjiang, Peoples R China.
通讯机构：
[Tang Guotao] U;Univ South China, Learning Key Lab Pharmacoprote, Inst Pharm & Pharmacol, Hengyang 421001, Hunan, Peoples R China.
关键词：
benzoic-imine bond;pH-sensitive;micelle;drug delivery system
摘要：
Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a known tumor suppressor in non-small cell lung cancer (NSCLC). By performing a systematic review and meta-analysis of the literature, we determined the prognostic value of decreased PTEN expression in patients with NSCLC. We comprehensively and systematically searched through multiple online databases up to May 22, 2016 for NSCLC studies reporting on PTEN expression and patient survival outcome. Several criteria, including the Newcastle-Ottawa Quality Assessment Scale (NOS), were used to discriminate between studies. In total, 23 eligible studies with a total of 2,505 NSCLC patients were included in our meta-analysis. Our results demonstrated that decreased expression of PTEN correlated with poor overall survival in NSCLC patients and was indicative of a poor prognosis for disease-free survival and progression-free survival in patients with NSCLC.
