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学者姓名：侯鹏
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Abstract ：
© 2018 Background: Previous studies indicated that miR-218 was deregulated in gastric cancer patients and correlated with tumor invasion and prognosis. The aim of this study was to clarify the effect of miR-218 on the malignant behavior of gastric cancer and its role in regulating Bmi-1/Akt signaling pathway. Materials and methods: We used miR-218 mimic to transfect gastric cancer cell lines AGS and SGC-7901, and the overexpression efficiency was validated using qRT-PCR assay. MTT assay and Transwell chamber system were performed to detect the effect of miR-218 on cell proliferation, invasion and migration on gastric cancer. Western blot and qRT-PCR assay was used to test the role of miR-218 in regulating Bmi-1/Akt signaling pathway. Results: As shown in our research, ectopic expression of miR-218 in gastric cancer cells inhibits the proliferation, invasion and migration of gastric cancer cells. In addition, miR-218 re-expression inhibits the expression of Bmi-1 and its downstream target p-Akt473, as well as MMPs and EMT process. Conclusions: miR-218 inhibits the proliferation, invasion and migration of gastric cancer cells through modulating EMT process and the expression of MMPs via Bmi-1/Akt signaling pathway.
Keyword ：
Akt Bmi-1 EMT Gastric cancer miR-218 MMPs
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| GB/T 7714 | Wu, Yongxing , Tian, Sijia , Chen, Yijun et al. miR-218 inhibits gastric tumorigenesis through regulating Bmi-1/Akt signaling pathway [J]. | Pathology Research and Practice , 2019 , 215 (2) : 243-250 . |
| MLA | Wu, Yongxing et al. "miR-218 inhibits gastric tumorigenesis through regulating Bmi-1/Akt signaling pathway" . | Pathology Research and Practice 215 . 2 (2019) : 243-250 . |
| APA | Wu, Yongxing , Tian, Sijia , Chen, Yijun , Ji, Meiju , Qu, Yiping , Hou, Peng . miR-218 inhibits gastric tumorigenesis through regulating Bmi-1/Akt signaling pathway . | Pathology Research and Practice , 2019 , 215 (2) , 243-250 . |
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目的 研究甲状腺癌中药物代谢基因CYP1A1、CYP1B1启动子区异常甲基化及其与临床病理特征之间的关系.方法 取201例甲状腺癌及23例正常甲状腺石蜡包埋组织基因组DNA,采用甲基化特异性PCR(MSP)检测上述基因启动子区甲基化状态,对比甲状腺乳头状癌(PTC)及正常对照中CYP1A1、CYP1B1基因甲基化的发生率.在体外实验中利用甲基化转移酶抑制剂5-氮-2′-脱氧胞苷(5-Aza-dC)处理5种甲状腺癌细胞系,用实时定量PCR(RT-PCR)方法检测5-Aza-dC处理前后CYP1A1、CYP1B1基因的表达变化.用logistic回归方法分析CYP1A1、CYP1B1基因的异常甲基化与临床特点之间的相关性.结果 在各种病理类型的甲状腺癌中均存在CYP1A1、CYP1B1基因甲基化的情况;在PTC中CYP1A1基因启动子区甲基化水平高于对照组,CYP1B1基因启动子区甲基化水平低于对照组;CYP1A1基因在PTC中的表达低于对照组(P<0.01),CYP1B1基因在PTC中的表达高于对照组(P<0.01);利用5-Aza-dC处理甲状腺癌细胞系后可使CYP1A1基因的表达水平在K1及C643细胞系中较对照分别升高6.92及8.30倍;CYP1B1基因在K1细胞中表达较对照升高7.62倍;CYP1B1基因启动子区甲基化与淋巴结转移呈负相关.结论 在PTC中基因启动子区甲基化调控CYP1A1及CYP1B1基因的表达,CYP1B1启动子区异常甲基化与PTC的淋巴结转移有关.
Keyword ：
CYP1A1 CYP1B1 DNA甲基化 甲状腺癌 聚合酶链反应
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| GB/T 7714 | 张利红 , 石静 , 郝文庆 et al. 甲状腺癌中CYP1A1和CYP1B1基因启动子区甲基化分析 [J]. | 中华内分泌代谢杂志 , 2018 , (8) : 667-673 . |
| MLA | 张利红 et al. "甲状腺癌中CYP1A1和CYP1B1基因启动子区甲基化分析" . | 中华内分泌代谢杂志 8 (2018) : 667-673 . |
| APA | 张利红 , 石静 , 郝文庆 , 田竹芳 , 祭美菊 , 侯鹏 et al. 甲状腺癌中CYP1A1和CYP1B1基因启动子区甲基化分析 . | 中华内分泌代谢杂志 , 2018 , (8) , 667-673 . |
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Background: Abnormal telomere length is widely reported in various human cancers, and it is considered to be an important hallmark of cancer. However, there is remarkably little consensus on the value of telomere length in the prognostic evaluation of esophageal cancers. Here, we attempted to determine the association of variable telomere length with clinical outcome of esophageal cancer patients. Materials and methods: Using real-time quantitative PCR, we examined relative telomere lengths (RTL) in a cohort of esophageal cancer and normal esophageal tissues, and statistically investigated the association between RTL and clinical outcomes of esophageal cancer patients. Results: The majority of esophageal cancers in this study had longer RTLs as compared to adjacent non tumor tissues. Enhanced tumor RTL was associated with smoking habit, poor differentiation, advanced tumor stage, lymph node metastasis and cancer related death. In particular, a close relationship between longer RTL and poor survival was fully demonstrated by using cox regression and Kaplan-Maier survival curves. Conclusions: We found frequent telomere elongation in esophageal cancer tissues, and demonstrated longer RTL may be an independent poor prognostic factor for esophageal cancer patients. (C) 2016 Elsevier GmbH. All rights reserved.
Keyword ：
Biomarker Clinical outcome Esophageal cancer Relative telomere length
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| GB/T 7714 | Lv, Yanyan , Zhang, Yong , Li, Xinru et al. Long telomere length predicts poor clinical outcome in esophageal cancer patients [J]. | PATHOLOGY RESEARCH AND PRACTICE , 2017 , 213 (2) : 113-118 . |
| MLA | Lv, Yanyan et al. "Long telomere length predicts poor clinical outcome in esophageal cancer patients" . | PATHOLOGY RESEARCH AND PRACTICE 213 . 2 (2017) : 113-118 . |
| APA | Lv, Yanyan , Zhang, Yong , Li, Xinru , Ren, Xiaojuan , Wang, Meichen , Tian, Sijia et al. Long telomere length predicts poor clinical outcome in esophageal cancer patients . | PATHOLOGY RESEARCH AND PRACTICE , 2017 , 213 (2) , 113-118 . |
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Increasing evidences have implicated somatic gain-of-function mutations at the telomerase reverse transcriptase (TERT) promoter as one of the major mechanisms that promote transcriptional activation of TERT and subsequently maintain telomere length in human cancers including glioma. To investigate the prognostic value of these mutations and telomere length, individually and their coexistence, in gliomas, we analyzed two somatic mutations C228T and C250T in the TERT promoter, relative telomere length (RTL), IDH1 mutation and MGMT methylation in 389 glioma patients, and explored their associations with patient characteristics and clinical outcomes. Our data showed that C228T and C250T mutations were found in 17.0% (66 of 389) and 11.8% (46 of 389) of gliomas, respectively, and these two mutations were mutually exclusive in this cancer. Moreover, they were significantly associated with WHO grade. We also found that the RTL was significant longer in gliomas than in meningiomas and normal brain tissues (Median, 0.89 vs. 0.44 and 0.50; P < 0.001), and demonstrated that the RTL was strongly correlated with tumor recurrence. Importantly, TERT promoter mutations or long RTL caused a significantly poorer survival than TERT wild-type or short RTL. Coexisting TERT promoter mutations and long RTL were more commonly associated with poor patient survival than they were individually. Notably, the patients with TERT promoter mutations particularly C228T or long RTL were resistant to radiotherapy. Collectively, TERT promoter mutations and long RTL are not only prognostic factors for poor clinical outcomes, but also the predictors of radiotherapy resistance in gliomas.
Keyword ：
glioma poor survival radiotherapy resistance relative telomere length TERT promoter mutations
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| GB/T 7714 | Gao, Ke , Li, Gang , Qu, Yiping et al. TERT promoter mutations and long telomere length predict poor survival and radiotherapy resistance in gliomas [J]. | ONCOTARGET , 2016 , 7 (8) : 8712-8725 . |
| MLA | Gao, Ke et al. "TERT promoter mutations and long telomere length predict poor survival and radiotherapy resistance in gliomas" . | ONCOTARGET 7 . 8 (2016) : 8712-8725 . |
| APA | Gao, Ke , Li, Gang , Qu, Yiping , Wang, Maode , Cui, Bo , Ji, Meiju et al. TERT promoter mutations and long telomere length predict poor survival and radiotherapy resistance in gliomas . | ONCOTARGET , 2016 , 7 (8) , 8712-8725 . |
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1. CYP1A2 is a highly polymorphic gene and CYP1A2 enzyme results in broad inter-individual variability in response to certain pharmacotherapies, while little is known about the genetic variation of CYP1A2 in Uyghur Chinese population. The aim of the present study was to screen Uyghur volunteers for CYP1A2 genetic polymorphisms. 2. We used DNA sequencing to investigate promoter, exons, introns, and 3' UTR of the CYP1A2 gene in 96 unrelated healthy Uyghur individuals. We also used SIFT (Sorting Intolerant From Tolerant) and PolyPhen-2 (Polymorphism Phenotyping v2) to predict the protein function of the novel non-synonymous mutation in CYP1A2 coding regions. 3. We identified 20 different CYP1A2 polymorphisms in the Uyghur Chinese population, including two novel variants (119A > G and 2410G > A). Variant 119A > G was predicted to be probably damaging on protein function by PolyPhen-2, by contrast, 2410G > A was identified as benign. The allele frequencies of CYP1A2*1A, *1B, *1F, *1G, *1J, *1M, *4, and *9 were 23.4%, 53.1%, 3.7%, 2.6%, 2.6%, 13.5%, 0.5%, and 0.5%, respectively. The frequency of *1F, a putative high inducibility allele, was higher in our sample population compared with that in the Caucasian population (p < 0.05). The most common genotype combinations were *1A/*1B (46.9%) and *1B/*1M (27.1%). 4. Our results provide basic information on CYP1A2 polymorphisms in Uyghur individuals and suggest that the enzymatic activities of CYP1A2 may differ among the diverse ethnic populations of the world.
Keyword ：
CYP1A2 ethnic groups genetic polymorphism Uyghur populations
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| GB/T 7714 | Geng, Tingting , Zhang, Xi Yang , Wang, Li et al. Genetic polymorphism analysis of the drug-metabolizing enzyme CYP1A2 in a Uyghur Chinese population: a pilot study [J]. | XENOBIOTICA , 2016 , 46 (6) : 542-547 . |
| MLA | Geng, Tingting et al. "Genetic polymorphism analysis of the drug-metabolizing enzyme CYP1A2 in a Uyghur Chinese population: a pilot study" . | XENOBIOTICA 46 . 6 (2016) : 542-547 . |
| APA | Geng, Tingting , Zhang, Xi Yang , Wang, Li , Wang, Huijuan , Shi, Xugang , Kang, Longli et al. Genetic polymorphism analysis of the drug-metabolizing enzyme CYP1A2 in a Uyghur Chinese population: a pilot study . | XENOBIOTICA , 2016 , 46 (6) , 542-547 . |
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Abstract ：
当前,我国医学研究生培养模式存在一些缺陷:学术型研究生的培养着重科研训练,不能充分了解临床工作的需求,不能提出具有前瞻性的应用基础研究课题;专业学位研究生主要以培养临床能力为主,但多缺乏必要的科研能力训练,缺乏科研思维,无法提出操作性强的科学问题,因而培养模式需要改革.本文提出在研究生教育中融入转化医学的理念和思维,旨在打破基础医学及临床医学之间的固有屏障,弥补基础科学研究与临床应用实践之间的鸿沟.实践证实该培养模式对培养全面型医学人才具有重要意义.
Keyword ：
学术型研究生 专业学位研究生 转化医学
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| GB/T 7714 | 赵真真 , 黄葶 , 崔巍 et al. 专业学位与学术型研究生转化医学教学模式的初探 [J]. | 西北医学教育 , 2015 , (6) : 985-987 . |
| MLA | 赵真真 et al. "专业学位与学术型研究生转化医学教学模式的初探" . | 西北医学教育 6 (2015) : 985-987 . |
| APA | 赵真真 , 黄葶 , 崔巍 , 侯鹏 , 施秉银 . 专业学位与学术型研究生转化医学教学模式的初探 . | 西北医学教育 , 2015 , (6) , 985-987 . |
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Abstract ：
当前,我国医学研究生培养模式存在一些缺陷：学术型研究生的培养着重科研训练,不能充分了解临床工作的需求,不能提出具有前瞻性的应用基础研究课题;专业学位研究生主要以培养临床能力为主,但多缺乏必要的科研能力训练,缺乏科研思维,无法提出操作性强的科学问题,因而培养模式需要改革。本文提出在研究生教育中融入转化医学的理念和思维,旨在打破基础医学及临床医学之间的固有屏障,弥补基础科学研究与临床应用实践之间的鸿沟。实践证实该培养模式对培养全面型医学人才具有重要意义。
Keyword ：
学术型研究生 专业学位研究生 转化医学
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| GB/T 7714 | 赵真真 , 黄葶 , 崔巍 et al. 专业学位与学术型研究生转化医学教学模式的初探 [J]. | 西北医学教育 , 2015 , (6) . |
| MLA | 赵真真 et al. "专业学位与学术型研究生转化医学教学模式的初探" . | 西北医学教育 6 (2015) . |
| APA | 赵真真 , 黄葶 , 崔巍 , 侯鹏 , 施秉银 . 专业学位与学术型研究生转化医学教学模式的初探 . | 西北医学教育 , 2015 , (6) . |
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Sulforaphane (SFN), a natural compound derived from broccoli/broccoli sprouts, has been demonstrated to be used as an antitumor agent in different types of cancers. However, its antitumor effect in thyroid cancer remains largely unknown. The aim of the study was to investigate the therapeutic potential of SFN for thyroid cancer and explore the mechanisms underlying antitumor effects of SFN by in vitro and in vivo studies. Our data demonstrated that SFN significantly inhibited thyroid cancer cell proliferation in a dose-and time-dependent manner, induced G2/M phase cell cycle arrest and apoptosis, and inhibited thyroid cancer cell migration and invasion by suppressing epithelial-mesenchymal transition (EMT) process and expression of Slug, Twist, MMP-2 and -9. Mechanically, SFN inhibited thyroid cancer cell growth and invasiveness through repressing phosphorylation of Akt, enhancing p21 expression by the activation of Erk and p38 signaling cascades, and promoting mitochondrial-mediated apoptosis via reactive oxygen species (ROS)-dependent pathway. Growth of xenograft tumors derived from thyroid cancer cell line FTC133 in nude mice was also significantly inhibited by SFN. Importantly, we did not find significant effect of SFN on body weight and liver function of mice. Collectively, we for the first time demonstrate that SFN is a potentially effective antitumor agent for thyroid cancer.
Keyword ：
reactive oxygen species (ROS) signaling pathways sulforaphane (SFN) thyroid cancer
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| GB/T 7714 | Wang, Liping , Tian, Zhufang , Yang, Qi et al. Sulforaphane inhibits thyroid cancer cell growth and invasiveness through the reactive oxygen species-dependent pathway [J]. | ONCOTARGET , 2015 , 6 (28) : 25917-25931 . |
| MLA | Wang, Liping et al. "Sulforaphane inhibits thyroid cancer cell growth and invasiveness through the reactive oxygen species-dependent pathway" . | ONCOTARGET 6 . 28 (2015) : 25917-25931 . |
| APA | Wang, Liping , Tian, Zhufang , Yang, Qi , Li, Heng , Guan, Haixia , Shi, Bingyin et al. Sulforaphane inhibits thyroid cancer cell growth and invasiveness through the reactive oxygen species-dependent pathway . | ONCOTARGET , 2015 , 6 (28) , 25917-25931 . |
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The protein tyrosine phosphatase 1B (PTP1B), a non-transmembrane protein tyrosine phosphatase, has been implicated in gastric pathogenesis. Several lines of recent evidences have shown that PTP1B is highly amplified in breast and prostate cancers. The aim of this study was to investigate PTP1B amplification in gastric cancer and its association with poor prognosis of gastric cancer patients, and further determine the role of PTP1B in gastric tumorigenesis. Our data demonstrated that PTP1B was significantly up-regulated in gastric cancer tissues as compared with matched normal gastric tissues by using quantitative RT-PCR (qRT-PCR) assay. In addition, copy number analysis showed that PTP1B was amplified in 68/131 (51.9%) gastric cancer cases, whereas no amplification was found in the control subjects. Notably, PTP1B amplification was positively associated with its protein expression, and was significantly related to poor survival of gastric cancer patients. Knocking down PTP1B expression in gastric cancer cells significantly inhibited cell proliferation, colony formation, migration and invasion, and induced cell cycle arrested and apoptosis. Mechanically, PTP1B promotes gastric cancer cell proliferation, survival and invasiveness through modulating Src-related signaling pathways, such as Src/Ras/MAPK and Src/phosphatidylinositol-3-kinase (PI3K)/Akt pathways. Collectively, our data demonstrated frequent overexpression and amplification PTP1B in gastric cancer, and further determined the oncogenic role of PTP1B in gastric carcinogenesis. Importantly, PTP1B amplification predicts poor survival of gastric cancer patients.
Keyword ：
Gastric cancer genomic amplification poor prognosis PTP1B signaling pathways
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| GB/T 7714 | Wang, Na , She, Junjun , Liu, Wei et al. Frequent amplification of PTP1B is associated with poor survival of gastric cancer patients [J]. | CELL CYCLE , 2015 , 14 (5) : 732-743 . |
| MLA | Wang, Na et al. "Frequent amplification of PTP1B is associated with poor survival of gastric cancer patients" . | CELL CYCLE 14 . 5 (2015) : 732-743 . |
| APA | Wang, Na , She, Junjun , Liu, Wei , Shi, Jing , Yang, Qi , Shi, Bingyin et al. Frequent amplification of PTP1B is associated with poor survival of gastric cancer patients . | CELL CYCLE , 2015 , 14 (5) , 732-743 . |
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5-Methylcytosine (5mC) can be converted to 5-hydroxymethylcytosine (5hmC) in mammalian DNA by the ten-eleven translocation (TET) enzymes. Traditional bisulfite-based DNA methylation analysis techniques have been widely used in the detection of 5mC. However, they can not discriminate 5hmC from 5mC, leading to overestimate 5mC levels. We here introduce a strategy, combination of selective oxidation and bisulfite pyrosequencing (BS-Pyroseq), for quantification of both 5mC and 5hmC at CpG sites within the promoters of CDH1, DAPK, RAR ss and RUNX3 genes in a panel of cell lines and clinical samples. As expected, oxidative bisulfite pyrosequencing (oxBS-Pyroseq) assay decreased overall or site-specific methylation levels of three of these genes in most cell lines as compared with BS-Pyroseq assay. Similarly, decreased overall or site-specific methylation levels of DAPK, RAR ss and RUNX3 genes in laryngeal, gastric and thyroid cancer and their matched normal tissues, respectively, were also found by a comparison between these two techniques, particularly in cancerous tissues. In addition, by using this combined strategy and hydroxymethylcytosine DNA immunoprecipitation (hMeDIP) assay, we demonstrated that TET1 up-regulated DAPK expression through promoter demethylation. Collectively, this strategy is easy to establish and accurately discriminates and quantifies 5mC and 5hmC at CpG sites within selected gene promoters.
Keyword ：
5-Hydroxymethylcytosine (5hmC) 5-Methylcytosine (5mC) Bisulfite Pyrosequencing Gene Promoter Selective Oxidation
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| GB/T 7714 | Qu, Yiping , Yang, Qi , Sui, Fang et al. A Strategy for Accurate Quantification of 5-Methylcytosine and 5-Hydroxymethylcytosine at CpG Sites Within Gene Promoter [J]. | JOURNAL OF BIOMEDICAL NANOTECHNOLOGY , 2015 , 11 (6) : 1016-1026 . |
| MLA | Qu, Yiping et al. "A Strategy for Accurate Quantification of 5-Methylcytosine and 5-Hydroxymethylcytosine at CpG Sites Within Gene Promoter" . | JOURNAL OF BIOMEDICAL NANOTECHNOLOGY 11 . 6 (2015) : 1016-1026 . |
| APA | Qu, Yiping , Yang, Qi , Sui, Fang , Lu, Rong , Dang, Siwen , Ji, Meiju et al. A Strategy for Accurate Quantification of 5-Methylcytosine and 5-Hydroxymethylcytosine at CpG Sites Within Gene Promoter . | JOURNAL OF BIOMEDICAL NANOTECHNOLOGY , 2015 , 11 (6) , 1016-1026 . |
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