Background Long noncoding RNAs (lncRNAs) have been reported as important molecules in cholangiocarcinoma (CCA) occurrence and development. A previous study showed that lncRNA GAS5 (GAS5) was an oncogene in some tumors. But the role of GAS5 in CCA progression reminds unclear. This research was designed to study the expression and potential effects of GAS5 in the progression of CCA. Methods The expression of GAS5 in CCA tissues was evaluated through mining of the TCGA and GEPIA databases. qRT-PCR was applied to validate the results in our clinical samples. χ2 test was used to analyze the association between the expression level of tissue GAS5 and different clinicopathological parameters of CCA patients. The target gene of GAS5 was predicted by bioinformatic databases, and further verified by luciferase reporter assays. Finally, the role of GAS5 in CCA cells invasion and proliferation was detected by Transwell assay and CCK-8 assay. Results Compared to the adjacent nontumor tissues and the normal human intrahepatic biliary epithelial cell, the expression of GAS5 was markedly increased in CCA tissues (p<0.001) and cell lines (p<0.01), respectively. CCA patients with high GAS5 expression tended to present lymph node metastasis (p<0.001) and had advanced clinical stage (p=0.006). The bioinformatics analysis predicted that hsa-miR-1297 was the potential target gene of GAS5, which was validated by luciferase reporter assays. In addition, the function study showed that GAS5 acted as a “sponge” to downregulate hsa-miR-1297, thus modulating CCA cell proliferation and invasion. Conclusion GAS5 acts as an endogenous sponge of hsa-miR-1297 to promote CCA cell proliferation and invasion, which might be a potential biomarker and therapeutic target for CCA.

*These authors contributed equally to this work Background: Long noncoding RNAs (lncRNAs) have been reported as important molecules in cholangiocarcinoma (CCA) occurrence and development. A previous study showed that lncRNA GAS5 (GAS5) was an oncogene in some tumors. But the role of GAS5 in CCA progression reminds unclear. This research was designed to study the expression and potential effects of GAS5 in the progression of CCA. Methods: The expression of GAS5 in CCA tissues was evaluated through mining of the TCGA and GEPIA databases. qRT-PCR was applied to validate the results in our clinical samples. χ test was used to analyze the association between the expression level of tissue GAS5 and different clinicopathological parameters of CCA patients. The target gene of GAS5 was predicted by bioinformatic databases, and further verified by luciferase reporter assays. Finally, the role of GAS5 in CCA cells invasion and proliferation was detected by Transwell assay and CCK-8 assay. Results: Compared to the adjacent nontumor tissues and the normal human intrahepatic biliary epithelial cell, the expression of GAS5 was markedly increased in CCA tissues (p<0.001) and cell lines (p<0.01), respectively. CCA patients with high GAS5 expression tended to present lymph node metastasis (p<0.001) and had advanced clinical stage (p=0.006). The bioinformatics analysis predicted that hsa-miR-1297 was the potential target gene of GAS5, which was validated by luciferase reporter assays. In addition, the function study showed that GAS5 acted as a “sponge” to downregulate hsa-miR-1297, thus modulating CCA cell proliferation and invasion. Conclusion: GAS5 acts as an endogenous sponge of hsa-miR-1297 to promote CCA cell proliferation and invasion, which might be a potential biomarker and therapeutic target for CCA.

MicroRNA-645 (miR-645) has been implicated in numerous types of human cancers including colon cancer. However, the effects and mechanisms of action of miR-645 dysregulation on the growth and malignancy of colorectal cancer (CRC) remain unclear. In this study, we demonstrated that miR-645 knockdown significantly diminished CRC cell migration and invasion and repressed epithelial-mesenchymal transition (EMT). Conversely, miR-645 overexpression enhanced CRC cell migration, invasion, and EMT. In vivo assays confirmed that miR-645 knockdown substantially reduced CRC growth and metastasis. Regarding the mechanism, ephrinA5 (EFNA5) was identified as a direct target gene of miR-645. MiR-645 specifically targeted the 3'-untranslated region of EFNA5 mRNA and hindered its expression. EFNA5 knockdown attenuated the effects of miR-645 knockdown on CRC cell migration and invasion. Additionally, we noted a statistically significant inverse correlation between EFNA5 mRNA and miR-645 levels in tumors from 28 patients with CRC. Hence, miR-645 acts as an oncogenic miRNA that may increase CRC cell migration, invasiveness, and metastasis by targeting EFNA5.

目的制备去甲斑蝥素（3-丙羧基）三苯基溴化膦（TPP）-聚乙二醇-b-聚己内脂（PEG-PCL）纳米胶束,研究其体外释放、细胞内转运及促肝肿瘤细胞凋亡作用。方法采用薄膜水化法制备去甲斑蝥素TPP-PEG-PCL纳米胶束,测定粒径、Zeta电位及显微电镜形态分析,同时对胶束进行稳定性、体外释放、药代动力学和临界胶束浓度测定;以香豆素-6作为荧光探针,评价TPP-PEG-PCL纳米胶束在肝肿瘤细胞内的摄取、溶酶体逃逸及线粒体靶向功能;采用给药剂量等同条件下,评价去甲斑蝥素TPP-PEG-PCL纳米胶束促肝肿瘤细胞凋亡效果。结果去甲斑蝥素TPP-PEG-PCL纳米胶束粒径为（16.8±0.2）nm,Zeta电位为（14.3±0.2）m V,透射电镜图片该纳米胶束呈规则圆球型;荧光试验结果显示,TPP-PEG-PCL纳米胶束可以促进药物的细胞摄取、逃逸溶酶体的捕获,最终靶向聚集在线粒体部位;细胞存活率和Hoechst染色结果显示去甲斑蝥素TPP-PEG-PCL纳米胶束具有很好的促肝肿瘤细胞凋亡作用,去甲斑蝥素TPP-PEG-PCL纳米胶束可以明显降低线粒体膜电位、提高细胞内活性氧（ROS）水平、增加促凋亡蛋白Bcl-2、减少抗凋亡Bax蛋白的表达,这些促凋亡相关的实验结果均明显优于去甲斑蝥素PEG-PCL纳米胶束和去甲斑蝥素,具有统计学意义。结论去甲斑蝥素TPP-PEG-PCL纳米胶束具有良好的肝肿瘤细胞线粒体靶向性和促肿瘤细胞凋亡作用,为一种潜在高效靶向肿瘤细胞线粒体的载药系统。

目的 研究青年胃癌(≤40岁)患者的临床病理特征及预后.方法 回顾性分析2011年1月至2012年12月在郑州大学附属肿瘤医院行手术治疗的胃癌患者,其中青年胃癌组(年龄≤40岁)110例,老年胃癌组(年龄≥60岁)720例,比较两组的临床病理特点及预后.结果 与老年胃癌患者相比,青年胃癌患者以女性常见,肿瘤大部分位于胃中下区,多见低分化腺癌、弥漫性胃癌,青年胃癌组有胃癌家族史的患者比例更高,而腹痛、呕血黑便等症状的比例低(P<0.05).两组在肿瘤大小、浸润深度、淋巴结转移、TNM分期及手术方式等方面比较,差异无统计学意义(P>0.05).单因素分析结果显示,肿瘤浸润深度、淋巴结转移、手术方式、TNM分期与术后生存时间有关(P<0.05).多因素分析提示,TNM分期及手术方式是影响青年胃癌患者预后的独立危险因素(HR=3.669,95％CI:1.590～8.468;HR=8.153,95％CI:3.657～18.180).结论 青年胃癌患者以女性为主,有其独特的临床病理特征,TNM分期及手术方式是其预后不良的独立危险因素.

S100 binding protein A16 (S100A16) expression levels are closely associated with microRNA (miRNA) processing. Higher levels of S100A16 are reported during the progression of many cancers. Our study mainly explored the interaction between S100A16 and miR-6884-5p in gastric cancer (GC). Quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the level of S100A16 and miR-6884-5p in GC tissues and cell lines. The si-S100A16, pcDNA-S100A16, miR-6884-5p mimic or inhibitor was transfected into GC cells, and the effects of S100A16 and miR-6884-5p on the proliferation, invasion, and epithelial‐mesenchymal transition (EMT) were explored by qRT-PCR and Western blot assays. Luciferase assays were performed to validate S100A16 as an miR-6884-5p target in GC cells. In our study, we found that the level of miR-6884-5p was significantly decreased and the expression of S100A16 was significantly increased in GC tissues and cell lines. There was a close association between these changes. Knockdown of S100A16 significantly inhibited the proliferation, invasion, and EMT of GC cells. The bioinformatics analysis predicted that S100A16 is a potential target gene of miR-6884-5p, and the luciferase reporter assay confirmed that miR-6884-5p could directly target S100A16. Introduction of miR-6884-5p to GC cells had similar effects to S100A16 silencing. Overexpression of S100A16 in GC cells partially reversed the inhibitory effects of the miR-6884-5p mimic. miR-6884-5p inhibited the proliferation, invasion, and EMT of GC cells by directly decreasing S100A16 expression.

Calixarene and its derivatives have extensively served as promising anti-tumor agents. Previously, we have synthesized a series of calix[n]arene polyhydroxyamine derivatives (n = 4, 6, 8) and found that 5,11,17,23-tetra-tert-butyl-25,27-bis [N-(2-hydroxyethyl)aminocarbonylmethoxyl] calix[4]arene (CLX-4) displayed significant effect toward SKOV3, A549, SW1990, HeLa, Raji, and MDA-MB-231 cancer cells. In the present work, we find a replacement of calix[4]arene bone and synthesized 19 novel structurally related dihomooxacalix[4]arene amide derivatives 4A-4S to optimize its efficacy. Their abilities to induce cytotoxicity in human lung carcinoma (A549) cells, breast cancer (MCF-7) cells, cervical cancer (HeLa) cells, hepatocellular carcinoma (HepG2) cells, as well as human umbilical vein endothelial (HUVEC) cells are evaluated in vitro. Encouraging results show that the majority of dihomooxacalix[4]arene amide derivatives are effective at inhibiting A549 cell proliferation with the corresponding IC50 ranging from 0.6 to 20.1 mu M. In particular, compounds 4A, 4D, and 4L explore markedly increased potency (IC50 value is 2.0 +/- 0.5 mu M, 0.7 +/- 0.1 mu M, and 1.7 +/- 0.4 mu M) over the cytotoxicity profiles of control CLX-4, whose IC50 value is 2.8 +/- 0.3 mu M. More interestingly, 4A also demonstrates the perfect cytotoxic effect against MCF-7, HeLa, and HepG2 cells with IC50 values of 1.0 +/- 0.1 mu M, 0.8 +/- 0.2 mu M, and 2.7 +/- 0.4 mu M. In addition, the results proved that our synthesized 4A has much lower toxicity (41%) to normal cells at a concentration of 10 mu M than that of 4D (90%). To reveal the mechanisms, the key indicators including the cell cycle and apoptosis are observed by the flow cytometry analysis in MCF-7 cells. The results demonstrate that both 4A and 4D can induce the MCF-7 cell cycle arrest in G0/G1 phase and cell apoptosis. Therefore, our finding proves that the dihomooxacalix[4]arene amide derivatives are convenient platforms for potential supramolecular anticancer agents.

目的 探究不同环氧合酶-2(COX-2)表达水平对胃癌细胞SGC-7901迁移能力及其上皮钙粘素(E-cadherin)表达的影响.方法 采用不同浓度的COX-2特异性抑制剂塞来昔布(10、20、30、40、50 μmol/L)干预胃癌细胞SGC-7901作为实验组,另设对照组(不加塞来昔布干预),构建不同COX-2表达水平的胃癌细胞SGC-7901,采用Transwell小室法检测胃癌细胞SGC-7901迁移情况.以终浓度为30 μmol/L的塞来昔布干预胃癌细胞SGC-7901,通过作用不同时间(24、36、48小时)构建不同COX-2表达水平的胃癌细胞SGC-7901,采用免疫荧光标记法检测胃癌细胞 SGC-7901 E-cadherin表达情况;采用实时荧光定量反转录PCR检测胃癌细胞SGC-7901 COX-2及E-cadherin mRNA表达情况.结果 对照组及实验组(10、20、30、40、50 μmol/L)COX-2 mRNA表达量分别为(1.00±0.00)及(0.82±0.15)、(0.70±0.29)、(0.62±0.25)、(0.49± 0.21)、(0.33±0.15);E-cadherin mRNA分别为(1.00±0.00)及(0.73±0.16)、(1.38±0.22)、(2.43±0.21)、(2.66±0.34)、(2.87±0.28).与对照组比较,实验组胃癌细胞SGC-7901 COX-2 mRNA表达量均显著降低, E-cadherin mRNA表达量显著升高,且均呈剂量依赖性(P<0.01).Transwell小室实验结果显示,与对照组比较,实验组胃癌细胞SGC-7901迁移数量均显著降低(P<0.01),实验组随COX-2表达水平的降低呈逐渐降低趋势(P<0.01),迁移抑制率呈逐渐升高趋势(P<0.01).以终浓度为30μmol/L塞来昔布处理胃癌细胞SGC-790124、36、48小时后COX-2 mRNA表达量分别为(0.69 ±0.23)、(0.55 ±0.17)、(0.42 ±0.11);E-cad-herin mRNA表达量分别为(2.46±0.23)、(4.03±0.31)、(5.11±0.28);SGC-7901 E-cadherin平均荧光强度分别为(21.25±4.32)、(27.67±5.01)、(46.38±4.92);随着塞来昔布作用时间的延长,胃癌细胞 SGC-7901 COX-2 mRNA表达量逐渐降低,而E-cadherin mRNA表达量及平均荧光强度均逐渐升高(P<0.05).结论通过COX-2特异性抑制剂塞来西布抑制胃癌细胞SGC-7901 COX-2表达,可显著上调其E-cadherin mRNA,进而抑制胃癌细胞SGC-7901迁移能力.

Objective To assess the value of serum carcinoembryonic antigen (CEA)and carbohydrate antigen 19-9 (CA19-9) levels in the diagnosis of gastric cancer in elderly patients.Methods This prospective study included 104 elderly patients with gastric cancer at our hospital from March 2015 to December 2016 to serve as an experimental group.Moreover,104 elderly patients with benign gastric lesions were enrolled to serve as a control group.Serum CEA and CA19-9 levels were compared between the two groups.The diagnostic specificity,sensitivity,and validity for gastric cancer were calculated by using CEA or CA19-9 alone or the two in combination.Results Serum CEA and CA19-9 levels in the experimental group were significantly higher than in the control group(t =3.001 and 5.110,P =0.039 and 0.016,respectively);The specificity,sensitivity,and validity of CEA and CA19-9 in combination were significantly higher than when each of the measures was used alone(x2 =2.101 and 2.109,P =0.031 and 0.019,respectively).Serum CEA levels showed good predictive power for both lymph node metastasis of gastric cancer(Z =5.109,P =0.002) and liver metastasis of gastric cancer(Z =3.910,P =0.026);Serum CA19-9 levels could predict lymph node metastasis of gastric cancer (Z =4.189,P =0.003) Conclusions Serum CEA and CA19-9 in combination have high sensitivity and validity for gastric cancer detection;Elevated CEA can predict gastric cancer metastasis and elevated CA19-9 may predict lymph node metastasis.

Objective:To analyze the short -term efficacy and toxic and side effects of concurrent chemoradiotherapy of Paclitaxel(PTX)combined with compound Kushen injection treating elderly patients with esophagus cancer.Methods:118 elderly patients with esophagus cancer were randomly divided into the observation group(n=59)and the control group(n=59).The control group was treated with concurrent chemoradiotherapy of PTX;on which basis,the observa-tion group was also treated with compound Kushen injection to the end of chemoradiotherapy.The chemoradiotherapy was three months,and the follow-up was one year.The short -term clinical efficacy was compared between the two groups;immune function changes before and after the treatment,as well as the toxic and side effects during the follow -up were observed.Results:After three-month treatment,DCR was 96.61%in the observation group,which was sig-nificantly higher than 67.80%in the control group(P<0.05);during the follow-up,the survival rate was 86.44%in the observation group,which was also significantly higher than 67.80% in the control group(P<0.05).The blood CD+4ratio and CD +4/CD+8were significantly higher after the treatment than those before the treatment in the theatment group;they were much higher in the observation group compared to those in the control group(P<0.01); the blood CD+8ratio after the treatment in the observation group was significantly lower than that before the treatment and that in the control group(P<0.01).The serum levels of IgG,IgA and IgM were significantly lower in the control group after the treatment than those before the treatment and those in the observation group(P<0.01).During the treatment and follow-up period,the toxic and side effects,such as the incidence rates of grade I ~II appetite,vomiting,white blood cell descent, radiation esophagitis and grade III ~IV vomiting, were remarkably lower in the observation group than those in the control group(P<0.05).Conclusion: Concurrent chemoradiotherapy of PTX combined with compound Kushen injection can effectively control the progress of esophagus cancer in elderly patients, reduce the toxic and side effects,and increase the tolerance and improve survival rate.

目的 评估阿瑞匹坦、奥氮平、托烷司琼与地塞米松四联止吐方案对接受高致吐性化疗方案治疗的女性乳腺癌患者的止吐效果.方法 选取2016年3月至2017年3月于郑州大学附属肿瘤医院乳腺科及肿瘤内科首次接受化疗的60例女性乳腺癌患者,所有患者均接受AC/EC方案化疗,按照随机数表法分为两组,各30例.试验组患者接受阿瑞匹坦、奥氮平、托烷司琼和地塞米松四联止吐方案;对照组接受托烷司琼和地塞米松二联止吐方案.比较两种方案的止吐效果.结果 两组患者急性期恶心、呕吐发生率及完全缓解率比较,差异无统计学意义(P>0.05);试验组患者延迟期恶心、呕吐发生率低于对照组,延迟期及总恶心、呕吐完全缓解率优于对照组,差异有统计学意义(P<0.05).治疗期间两组患者均未观察到Ⅲ～Ⅳ级不良反应,试验组患者嗜睡发生率高于对照组,差异有统计学意义(P<0.05),两组其他不良反应发生率比较,差异无统计学意义(P>0.05).结论 四联止吐方案用于接受高致吐性化疗方案治疗的女性乳腺癌患者,可降低患者的恶心、呕吐发生率,缓解患者的恶心、呕吐症状,且不良反应发生率低,患者可耐受.

OBJECTIVE:To explore genes potentially co-expressed with cyclin E in gastric cancer and discover possible targets for gastric cancer treatment.METHODS:The Cancer Genome Atlas (TCGA) stomach adenocarcinoma sequencing data were used to predict genes co-expressed with cyclin E. Co-expression genes predicted by cBioPortal online analysis with Pearson correlation coefficient ≥0.4 were analyzed by gene ontology (GO) enrichment annotation using the PANTHER online platform (Ver. 7). Interactions between proteins encoded by these genes were analyzed using the STRING online platform (Ver. 10.5) and Cytoscape software (Ver. 3.5.1). Genes displaying a high degree of connection were analyzed by transcription factor enrichment prediction using FunRich software (Ver. 3). The significant transcription factor and cyclin E expression levels and their impact on gastric cancer progression were analyzed by Western blotting and Kaplan-Meier survival curve analysis.RESULTS:After filtering the co-expression gene prediction results, 78 predicted genes that included 73 protein coding genes and 5 non-coding genes with Pearson correlation coefficient ≥0.4 were selected. The expressions of the genes were considered to be correlated with cyclin E expression. Among the 78 genes co-expressed with cyclin E, 19 genes at the central of the regulatory network associated with cyclin E were discovered. Nuclear transcription factor Y subunit alpha (NF-YA) was identified as a significant transcription factor associated with cyclin E co-expressing genes. Analysis of specimen donors' clinical records revealed that high expression of NF-YA tended to be associated with increased cyclin E expression. The expression of both was associated with progression of gastric cancer. Western blotting results showed that compared with normal tissues, NF-YA and cyclin E were highly expressed in tumor tissues (P < 0.001). Survival curve analysis clearly demonstrated relatively poor overall survival of gastric cancer patients with high cyclin E or high NF-YA expression level, compared to patients with low cyclin E or NF-YA expression (P < 0.05).CONCLUSIONS:NF-YA may promote gastric cancer progression by increasing the transcription of cyclin E and other cell cycle regulatory genes. NF-YA might be a potential therapeutically useful prognostic factor for gastric cancer.

miRNAs were reported as oncogene or tumour suppressors in various cancers and played important roles in tumour development and progression. Dysregulated miR-133 has been reported in several cancers, however, the expression and biological function of miR-133 in glioma remained unclear. In this study, we found that miR-133 expression level was significantly decreased in glioma tissues and cell lines by RT-qPCR. Then miR-133 mimics were used to evaluate the effects of miR-133 on cell proliferation and invasion in vitro. We found that overexpressed miR-133 could significantly suppress cell growth, and invasion in U87 cells. Additionally, we found that forkhead box C1 (FOXC1) was overexpressed in glioma tissue and it was directly regulated by miR-133. Overall, this study is the first proof to demonstrate that miR-133 function as tumour suppressor in glioma and inhibit cell proliferation and invasioned by directly targeting FOXC1, implying miR-133 as a potential therapeutic target for glioma.

目的:探讨评价对进展期胃癌患者实施奥沙利铂联合卡培他滨化疗的临床效果.方法:选取2009年1月至2014年1月郑州大学附属肿瘤医院收治的进展期胃癌患者168例展开临床研究,按照随机数字表分为两组,分别实施常规治疗(常规组,n=84)和奥沙利铂联合卡培他滨治疗(研究组,n=84).比较两组患者临床获益率、不同时刻生存率.结果:两组患者临床获益率比较,差异具有统计学意义(P＜0.05);研究组患者治疗后2年、3年生存率远高于常规组,差异具有统计学意义(P＜0.05).结论:对进展期胃癌患者实施奥沙利铂联合卡培他滨治疗效果良好,能有效改善远期生存率.

The Regorafenib is a broad-spectrum kinase inhibitor that has been approved to treat colorectal cancer (CRC). However, evidences have shown that the agent is also implicated in drug interaction with microRNA-21 (miR-21), an oncogenic miRNA which plays a key role in resisting programmed cell death in CRC cells. Here, we supposed that, instead of kinase inhibition, Regorafenib can directly bind to and then stabilize miR-21 pre-element, thus preventing RNase Dicer-meditated cleavage of the pre-element to mature miR-21. In order to verify the notion, an in silico-in vitro integrated investigation of the direct intermolecular interaction between Regorafenib and miR-21 pre-element was performed by using active pocket identification, RNA–ligand docking, molecular dynamics (MD) simulation, binding energetic analysis, and fluorescence-based assay. It was revealed that the Regorafenib can bind at the major groove-like stem region of miR-21 pre-element through three geometrically satisfactory hydrogen bonds (H-bonds) as well as a number of hydrophobic forces and π-π stacking, conferring strong specificity and high stability to the RNA–ligand complex system (Kd = 0.73 μM). Separate inversion mutation of two base pairs (G6C, C12G) and (A13U, U4A) that are involved in the H-bonding can considerably impair the affinity of Regorafenib to miR-21 pre-element, with Kd increase to 27 and 96 μM, respectively. All these supported that Regorafenib can directly bind to miR-21 pre-element at molecular level and the binding mode can be properly modeled by using the proposed integrated strategy. This study would provide a potential, alternative mechanism for anti-colorectal cancer chemotherapy with Regorafenib.

目的 探讨长链非编码RNA脑细胞质RNA1 (Brain Cytoplasmic RNA 1,BCYRN1)在食管鳞状细胞癌(Esophageal Squamous Cell Carcinoma,ESCC)中的表达及其预后意义.方法 应用实时荧光定量PCR检测70例接受根治术治疗的ESCC患者癌组织及对应癌旁组织中BCYRN1的表达水平,并分析BCYRN1相对表达水平与ESCC患者临床病理特征及预后的关系.结果 ①与癌旁组织相比,BCYRN1在57.1％ (40/70)的ESCC癌组织中表达上调,且ESCC癌组织中BCYRN1表达水平明显增高(t=2.325,P=0.023).②BCYRN1的相对表达水平与患者临床病理因素如年龄、临床病理分期及组织学分级等均无关.③Kaplan-Meier生存分析显示BCYRN1高表达组患者的疾病无进展时间(Disease Free Survival,DFS)及总生存时间(Overall Survival,OS)显著缩短(x2=4.488,P=0.034和x2=4.629,P=0.031).多因素回归分析临床病理特征及BCYRN1表达水平对DFS和OS的影响结果显示,BCYRN1表达水平对DFS和OS的风险比(HR)分别为2.165 (95％ CI:1.119-4.186,P=0.022)和2.242(95％ CI:1.120 ～4.488,P=0.023).结论 BCYRN1高表达与预后差有关,可能是接受根治术治疗的ESCC患者的预后指标.

Calixarene-based compounds are highly effective therapeutic agents against cancer. This study aims to prepare a series of calix [n]arene (n = 4, 6, 8) polyhydroxyamine derivatives (3a-3m) and to study their potential antitumor activities. The single crystal structure of calixs[4]arene derivative 3a was determined through X-ray diffraction. We assessed the ability of the prepared calix [n]arene polyhydroxyamine derivatives to induce cytotoxicity in six cancer cell lines by performing cancer cell growth inhibition assays. Results demonstrated that compounds 3a-3d achieved IC50 values ranging from 1.6 mu M to 113 mu M. Among the different compounds, 3a and 3b exerted the strongest cytotoxic effect in inhibiting the growth of SKOV3 cells. In relation to the underlying mechanisms of cytotoxic effects, cell cycle analysis revealed that the exposure of SKOV3 cells to 3a induced cell cycle arrest in the G0/G1 phase, suggesting a reduction in DNA synthesis. Immunofluorescent staining indicated that the protein expression levels of caspase-3 and p53 in cells significantly increased, whereas that of Bcl-2 was effectively suppressed. Meanwhile, no significant changes in Bax were observed in SKOV3 cells. These results highlight that calixarene 3a can be further studied as a potential anticancer agent. (C) 2016 Elsevier Masson SAS. All rights reserved.

Objective To evaluate the clinical effect and the cost-effectiveness of three epidermal growth factor receptor-tyrosine kinase inhibitors(EGFR-TKI)in the treatment of advanced non-small cell lung cancer for the pur-pose of higher quality medical care. Methods The 118 patients with non-small cell lung cancer received the EG-FR-TKI treatment were divided into three groups:the erlotinib group(n = 38),the gefitinib group(n = 43)and the icotinib group(n = 37). The efficacy of the three drugs was evaluated. Pharmacoeconomic cost-effectiveness analysis was used to evaluate three drugs. Results The effective rates of the erlotinib group,the gefitinib group and the ico-tinib group were 71. 05% ,74. 42% and 67. 57%(P > 0. 05),respectively. There was no statistical difference in the toxicities among the three groups(P > 0. 05). The cost-effectiveness ratio of the erlotinib group,the gefitinib group and the icotinib group were 268. 30,201. 63 and 182. 28,respectively,the icotinib group was significantly lower than the erlotinib group and the gefitinib groups. Conclusion Three EGFR-TKI are safe and effect in the treatment of advanced non-small cell lung cancer,icotinib is the most economical EGFR-TKI protocol.

目的:研究肝癌患者BANCR的表达与其临床病理参数的关系,并探讨BANCR与E-cadherin、Vimentin表达的相关性.方法:应用荧光实时定量PCR(real-time quantitative PCR,qRT-PCR)检测BANCR在108例肝癌和癌旁组织中表达水平,免疫组织化学技术检测E-cadherin、Vimentin标记蛋白在肝癌组织中的表达情况,统计分析BANCR表达与临床病理特征之间关系及其与E-cadherin、Vimentin表达的相关性.结果:BANCR在82.4％(89/108)的肝癌组织中表达上调,其相对表达量为1.95±0.89,高于癌旁组织的0.86±0.54,差异有统计学意义(P＜0.05).BANCR的表达水平与淋巴结转移和AJCC分期明显相关(P＜0.05),而与性别、年龄、甲胎蛋白、肿瘤的大小、肿瘤数目、血管侵袭及Edmondson-Steiner病理分级无明显统计学差异(P＞0.05).通过Spearman等级相关分析,BANCR的表达与Vimentin的表达呈正相关(r=0.459,P＜0.05),与E-cadherin的表达呈负相关(r=-0.492,P＜0.05).结论:BANCR在肝癌组织中高表达,可能参与肝癌的发生发展和转移;BANCR与E-cadherin、Vimentin表达具有相关性.

Ohjeetive To observe the short-term efficacy and toxic reaction of compound sophora flavescens injection in the treatment of advanced colorectal carcinoma.Methods From January 2012 to April 2014,78 patients with advanced colorectal carcinoma were randomly divided into observation group and control group,with 39 cases in each group.The patients in the observation group were given compound sophora flavescens injection and XELOX chemotherapy,and the patients in the control group were given XELOX chemotherapy alone.Twenty-one days was as one cycle and the treatment course lasted for four cycles.Toxic reaction,quality of life,therapeutic efficiency,and clinical symptom were observed after the treatment.Results There was no significant difference in the tumor response rate and the level of CEA between the two groups (P ＞0.05).The KPS scores were significantly improved in chemotherapy group compared with chemotherapy control group (P ＜ 0.05).In addition,the incidences of gastrointestinal reaction and myelosuppression were lower than those in the control group (P ＜ 0.05).Conclusions Compound sophora flavescens injection combined with chemotherapy in the treatment of advanced colorectal carcinoma can reduce toxic reaction of chemotherapy and improve the quality of life in patients with advanced colorectal carcinoma,so it is worthy to be popularized.