检索结果-南通市图书馆

Regulatory mechanisms for abnormal expression of the human breast cancer specific gene 1.in breast cancer cells

Science china({1.fe Sciences) 2006年第4期49卷 403-408页

作者： lu aiping1,{1., liu jingwen2 1. department of pathology, peking university school of oncology, beijing cancer hospital, beijing 100036, china 2. VA Palo alto Health Care System, Palo Alto, California, CA 94304, USA department of {1. Peking University School of Oncology Beijing Cancer Hospital Beijing 100036 China VA Palo alto Health Care System Palo Alto California CA 94304 USA

Breast cancer-specific gene 1.(BCSG1., also referred as synuclein γ, was originally iso-lated from a human breast cancer cDNA library and the protein is mainly localized to presynaptic terminals in the nervous system. BCSG1.is not expressed in normal or benign breast lesions, but expressed at an extremely high level in the vast majority of the advanced staged breast carcinomas and ovarian carcinomas. Overexpression of BCSG1.in cancer cells led to significant increase in cell proliferation, motility and invasiveness, and metastasis. To elucidate the molecular mechanism and regulation for abnormal transcription of BCSG1. a variety of BCSG1.promoter luciferase reporters were constructed including 3′ end deleted sequences, Sp1.deleted, and activator protein-1.(AP1. domains mutated. Transient transfection assay was used to detect the transcriptional activation of BCSG1.promoters. Results showed that the Sp1.sequence in 5′-flanking region was involved in the basal transcriptional activities of BCSG1.without cell-type specificity. In comparison to pGL3-1.49, the reporter activities of pGL3-1.53 in BCSG1.negative MCF-7 cells and pGL3-1.59 in HepG2 cells were notably decreased. Mutations at AP1.sites in BCSG1.intron 1.significantly reduced the promoter ac-tivity in all cell lines. Transcription factors, c-jun, c-fos and cyclin AMP-responsive element binding (CREB) protein, could markedly enhance the promoter activities. Thus, our results suggest that the abnormal expression of BCSG1.in breast cancer cells is likely regulated by multiple mechanisms. The 5′ flanking region of BCSG1.provides the basal transcriptional activity without cell type specificity. A critical promoter element involved in abnormal expression of BCSG1.presents in the first exon. The cell type specificity of BCSG1.transcription is probably affected through intronic cis-regulatory se-quences. AP1.domains in the first intron play an important role in control of BCSG1.transcription.

关键词： breast cancer-specific gene 1. promoter, transcriptional activity.

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Decitabine induces IRF7-mediated immune responses in p53-mutated triple-negative breast cancer:a c{1.nical and translational study

引用

Frontiers of Medicine 2024年第2期18卷 357-374页

作者： Haoyu Wang Zhengyuan Wang Zheng Wang Xiaoyang li Yuntong li Ni Yan lili Wu Ying liang Jiale Wu Huaxin Song qing Qu Jiahui Huang Chunkang Chang Kunwei Shen Xiaosong Chen Min lu department of General Surgery Comprehensive Breast Health CenterRuijin Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghai200025China Shanghai Institute of Hematology State Key Laboratory of Medical GenomicsNational Research Center for Translational Medicine(Shanghai)Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghai200025China department of Hematology Shanghai Institute of HematologyRuijin Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghai200025China department of Hematology Shanghai Jiao Tong University Affiliated Sixth People’s HospitalShanghai200025China

p53 is mutated in half of cancer ***,no p53-targeting drugs have been ***,we reposition decitabine for triple-negative breast cancer(TNBC),a subtype with frequent p53 mutations and extremely poor *** a retrospective study on tissue microarrays with 1.2 TNBC cases,DNMT1.overexpression was associated with p53 mutations(P=0.037)and poor overall survival(OS)(P=0.01.).In a prospective DEciTabinE and Carboplatin in TNBC(DETECT)trial(NCT03295552),decitabine with carboplatin produced an objective response rate(ORR)of 42%in 1. patients with stage IV *** the 9 trialed patients with available TP53 sequencing results,the 6 patients with p53 mutations had higher ORR(3/6 vs.0/3)and better OS(1..0 vs.4.0 months)than the patients with wild-type *** a mechanistic study,isogenic TNBC cell lines harboring DETECT-derived p53 mutations exhibited higher DNMT1.expression and decitabine sensitivity than the cell line with wild-type *** the DETECT trial,decitabine induced strong immune responses featuring the striking upregulation of the innate immune player IRF7 in the p53-mutated TNBC cell line(upregulation by 1.-fold)and the most responsive patient with *** integrative studies reveal the potential of repurposing decitabine for the treatment of p53-mutated TNBC and suggest IRF7 as a potential biomarker for decitabine-based treatments.

关键词： p53 mutation triple-negative breast cancer decitabine DNMT1 IRF7 innate immune response

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Gum mastic increases maspin expression in prostate cancer cells

引用

Acta Pharmacologica Sinica 2007年第4期28卷 567-572页

作者： Mei-lan HE~(2,3,6),Wei-wen CHEN~(2,6),Peng-ju ZHANG~2,An-li JIANG~2,Wei FAN~4,Hui-qing YUAN~2,Wen-wen liu~2,Jian-yeZHANG~(2,5)~2department of Biochemistry,Medical school,Shandong university,Ji-nan 250012,china ~3Institute of cancer Research,life Science andTechnology school,Tongji university Shanghai 200092,china ~4Gastric Intestine department,Affiliated Qi-lu hospital,Shandong university,Ji-nan 250012,china department of Biochemistry Medical School Shandong University Ji-nan China Institute of cancer Research Life Science and Technology School Tongji University Shanghai China Gastric Intestine department Affiliated Qi-Lu Hospital Shandong University Ji-nan China

Aim:To study whether gum mastic,a natural resin,can regulate maspin expres-sion in prostate cancer cells,and further investigate the mechanisms involved inthis regulatory ***:RT-PCR and Western blotting were used todetect maspin expression at the transcriptional and translational *** assay was used to investigate the effect of gum mastic on the maspin *** binding activity of negative androgen-responsive element (ARE) and posi-tive Spl element in the maspin promoter were studied by electrophoretic mobi{1.tyshift ***:Gum mastic induced maspin mRNA and protein expression,and the maspin promoter activity was enhanced with gum mastic ***,gum mastic inhibited the ARE binding activity and increased the Sp 1.bindingactivity in the maspin ***:Gum mastic enhances maspin pro-moter activity by suppressing ARE binding activity and enhancing Spl bindingactivity,and the increased activity in the maspin promoter finally leads to the up-regulation of both its mRNA and protein levels.

关键词： gum mastic maspin expression ARE binding activity Spl binding activity

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Alterations of tumor-related genes do not exactly match the histopathological grade in gastric adenocarcinomas

引用

World Journal of Gastroenterology 2010年第9期16卷 1129-1137页

作者： Guo-Yan liu,Xiao-Hong Wu,Yi-Zhuo lu,Chao Pan,Ping Yin,Hong-Feng liao,Ji-Qin Su,qing Ge,Qi luo,department of General Surgery,The Affiliated Zhongshan hospital of Xiamen university,The Digestive Disease Research Institute of Xiamen university,Xiamen 361004,Fujian Province,china Guo-Yan liu,Bin Xiong,department of oncology,The Affiliated Zhongnan hospital of Wuhan university,Wuhan 430071,Hubei Province,china Kun-Hong liu,department of Data Mining,Software school of Xiamen university,Xiamen 361005,Fujian Province,china Yong Zhang,Yu-Zhi Wang,The Academy of Military Medical Sciences,beijing 100850,china department of General Surgery The Affiliated Zhongshan Hospital of Xiamen University The Digestive Disease Research Institute of Xiamen University Xiamen 361004 Fujian Province China.

AIM:To investigate the diverse characteristics of different pathological gradings of gastric adenocarcinoma (GA) using tumor-related ***:GA tissues in different pathological gradings and normal tissues were subjected to tissue *** of 1. major tumor-related genes were detected by RNA in situ hybridization along with 3' terminal digoxin-labeled anti-sense single strandedoligonucleotide and locked nucleic acid modifying probe within the tissue *** data obtained were processed by support vector machines by four different feature selection methods to discover the respective critical gene/gene subsets contributing to the GA activities of different pathological ***:In comparison of poorly differentiated GA with normal tissues,tumor-related gene TP53 plays a key role,although other six tumor-related genes could also achieve the Area Under Curve (AUC) of the receiver operating characteristic independently by more than 80%.Comparing the well differentiated GA with normal tissues,we found that 1. tumor-related genes could independently obtain the AUC by more than 80%,but only the gene subsets,TP53,RB and PTEN,play a key *** the gene subsets,Bcl1.,UVRAG,APC,Beclin1.NM23,PTEN and RB could distinguish between the poorly differentiated and well differentiated *** of a single gene could obtain a valid ***:Different from the traditional point of view,the well differentiated cancer tissues have more alterations of important tumor-related genes than the poorly differentiated cancer tissues.

关键词： Pathological grading Gastric adenocarcinoma Tumor-related gene Support vector machine RNA in situ hybridization

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Dosimetric risk factors for radiation esophagitis in patients with breast cancer following regional nodal radiation

引用

World Journal of Clinical Cases 2024年第17期12卷 2995-3003页

作者： Mei-Chen Ji Zhi-Jia li Ke li Yun-Xiao Wang Bo Yang lin-lin Lv Ying Su Zhi-Wei Zhang Zhong-Chao Huo qing Qi Yong-Chang lu Zhi-Qiang Cui Yan-Bao liu oncology Center The Affiliated Hospital of Hebei University of EngineeringHandan 056002Hebei ProvinceChina General Surgery department Handan First HospitalHandan 056002Hebei ProvinceChina department of Breast Surgery The Affiliated Hospital of Hebei University of EngineeringHandan 056002Hebei ProvinceChina school of C{1.nical Medicine Hebei University of EngineeringHandan 056002Hebei ProvinceChina

BACKGROUND Radiation esophagitis(RE)is one of the most common clinical symptoms of regional lymph node radiotherapy for breast ***,there are fewer studies focusing on RE caused by hypofractionated radiotherapy(HFRT).AIM To analyze the clinical and dosimetric factors that contribute to the development of RE in patients with breast cancer treated with HFRT of regional lymph *** Between January and December 2022,we retrospectively analysed 64 patients with breast cancer who met our inclusion criteria underwent regional nodal intensity-modulated radiotherapy at a radiotherapy dose of 43.5 Gy/*** Of the 64 patients in this study,24(37.5%)did not develop RE,29(45.3%)developed grade 1.RE(G1.E),1.(1..2%)developed grade 2 RE(G2RE),and none developed grade 3 RE or *** univariable logistic regression analysis found G2RE to be significantly correlated with the maximum dose,mean dose,relative volume 20-40,and absolute volume(AV)*** stepwise linear regression analyses found AV30 and AV35 to be significantly associated with G2RE(P1..The optimal threshold for AV30 was 2.39 mL[area under the curve(AUC):0.996;sensitivity:90.9%;specificity:91.1.].The optimal threshold for AV35 was 0.71.mL(AUC:0.932;sensitivity:90.9%;specificity:83.9%).CONCluSION AV30 and AV35 were significantly associated with *** thresholds for AV30 and AV35 should be limited to 2.39 mL and 0.71.mL,respectively.

关键词： Breast cancer Dosimetric parameters Radiation esophagitis Esophagitis Hypofractionated radiotherapy

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

To explore the mechanism of Yigong San anti-gastric cancer and immune regulation

引用

World Journal of Gastrointestinal oncology 2024年第5期16卷 1965-1994页

作者： Dou-Dou lu {1.ng Yuan Zhao-Zhao Wang Jian-Jun Zhao Yu-Hua Du Na Ning Guo-qing Chen Shi-Cong Huang Yi Yang Zhe Zhang Yi Nan school of C{1.nical Medicine Ningxia Medical UniversityYinchuan 750004Ningxia Hui Autonomous RegionChina College of Pharmacy Ningxia Medical UniversityYinchuan 750004Ningxia Hui Autonomous RegionChina Traditional Chinese Medicine College Ningxia Medical UniversityYinchuan 750004Ningxia Hui Autonomous RegionChina department of Chinese Medical Gastrointestinal China-Japan Friendship HospitalBeijing 100029China Key Laboratory of Ningxia Minority Medicine Modernization Ministry of Education Ningxia Medical UniversityYinchuan 750004Ningxia Hui Autonomous RegionChina

BACKGROUND Yigong San(YGS)is a representative prescription for the treatment of digestive disorders,which has been used in clinic for more than 1.00 ***,the mechanism of its anti-gastric {1. and regulate immunity are still remains *** To explore the mechanism of YGS anti-gastric {1. and immune *** Firstly,collect the active ingredients and targets of YGS,and the differentially expressed genes of gastric ***,constructed a protein-protein interaction network between the targets of drugs and diseases,and screened hub *** the clinical relevance,mutation and repair,tumor microenvironment and drug sensitivity of the hub gene were ***,molecular docking was used to verify the binding ability of YGS active ingredient and hub *** Firstly,obtained 55 common targets of gastric {1. and *** Kyoto Encyclopedia of Genes and Genomes screened the microtubule-associated protein kinase signaling axis as the key pathway and IL6,EGFR,MMP2,MMP9 and TGFB1.as the hub *** 5 hub genes were involved in gastric carcinogenesis,staging,typing and prognosis,and their mutations promote gastric {1. ***,molecular docking results confirmed that the components of YGS can effectively bind to therapeutic *** YGS has the effect of anti-gastric {1. and immune regulation.

关键词： Gastric cancer Yigong San Mechanism Immune

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

MiR-6838-5p过表达下调DDR1.因表达抑制乳腺癌MCF-7细胞的增殖

引用

南方医科大学学报 2024年第9期44卷 1677-1684页

作者：薛良军谈秋瑜许静文冯璐李文锦颜亮李玉磊皖南医学院第一附属医院放疗科安徽芜湖241002 皖南医学院基础医学院安徽芜湖241002

目的探索miR-6838-5p调控DDR1.因表达水平对乳腺癌MCF-7细胞增殖的影响。方法采用脂质体转染方法干预乳腺癌MCF-7细胞中miR-6838-5p及DDR1.因表达,设置组别如下:Control mimic;miR-6838-5p mimic;Control inhibitor;miR-6838-5p inhibitor;Control siRNA、DDR1.siRNA、Control vector、DDR1.vector及miR-6838-5p过表达+DDR1.表达共转染组。qRT-PCR实验检测miR-6838-5p在正常乳腺上皮细胞及乳腺癌细胞中的表达;通过TargetscanV 8.0等软件预测miR-6838-5p可能作用的靶基因;双荧光素酶报告基因实验验证miR-6838-5p与DDR1.在靶向结合位点;CCK-8实验及EdU实验检测细胞增殖情况;Western blotting实验检测DDR1.达情况;通过裸鼠荷瘤实验验证miR-6838-5p通过调控DDR1.达抑制了乳腺癌MCF-7细胞增殖。结果miR-6838-5p在乳腺癌细胞中表达量低于乳腺正常上皮细胞(P1.P1.,Western blotting实验证明miR-6838-5p能调控DDR1.因表达;DDR1.进乳腺癌细胞的增殖(P1.表达共转染后能回复miR-6838-5p对乳腺癌细胞增殖的抑制作用(P1.表达(P1.因表达抑制了乳腺癌细胞的增殖。

关键词： miR-6838-5p 乳腺癌 DDR1 细胞增殖

来源：

维普期刊数据库

同方期刊数据库博看期刊评论

在线全文

学校读者我要写书评

暂无评论

Downregulation of MEIS1.mediated by ELFN1.AS1.EZH2/DNMT3a axis promotes tumorigenesis and oxaliplatin resistance in colorectal {1.

引用

Signal Transduction and Targeted Therapy 2022年第4期7卷 1343-1355页

作者： Yimin li Yaqi Gan Jiaxin {1. Juanni li Zhengwei Zhou Ruotong Tian Ruizheng Sun Jiaqi {1. qing Xiao Yuanyuan li Pengyan lu Yulong Peng Yuqian Peng Guang Shu Gang Yin department of {1. Xiangya HospitalSchool of Basic Medical SciencesCentral South UniversityChangshaChina school of Basic Medical Sciences Central South UniversityChangshaHunan ProvinceChina department of Microbiology School of Basic Medical ScienceCentral South UniversityChangshaChina china-Africa Research Center of Infectious Diseases School of Basic Medical SciencesCentral South UniversityChangshaHunan ProvinceChina

Oxaliplatin is widely used in the frontline treatment of colorectal cancer(CRC),but an estimated 50%of patients will eventually stop responding to treatment due to acquired *** study revealed that diminished MEIS1.expression was detected in CRC and harmed the survival of CRC ***1.impaired CRC cell viabilities and tumor growth in mice and enhanced CRC cell sensitivity to oxaliplatin by preventing DNA damage ***,oxaliplatin resistance following MEIS1.suppression was critically dependent on enhanced FEN1.***,we confirmed that EZH2-DNMT3a was assisted by lncRNA ELFN1.AS1.in locating the promoter of MEIS1.to suppress MEIS1.transcription *** on the above,therapeutics targeting the role of MEIS1.in oxaliplatin resistance were developed and our results suggested that the combination of oxaliplatin with either ELFN1.AS1.ASO or EZH2 inhibitor GSK1.6 could largely suppress tumor growth and reverse oxaliplatin *** study highlights the potential of therapeutics targeting ELFN1.AS1.and EZH2 in cell survival and oxaliplatin resistance,based on their controlling of MEIS1.expression,which deserve further verification as a prospective therapeutic strategy.

关键词： EZH2 impaired resistance

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

NDFIP1.limits cel{1.lar TAZ accumulation via exosomal sorting to inhibit NSCLC proliferation

引用

Protein & Cell 2023年第2期14卷 123-136页

作者： Yirui Cheng Xin lu Fan {1. Zhuo Chen Yanshuang Zhang qing Han qingyu Zeng Tingyu Wu Ziming {1. Shun lu Ceci{1.a Wil{1.ams Wei{1.ang Xia State Key Laboratory of Oncogenes and Related Genes Ren Ji HospitalSchool of Medicine and School of Biomedical EngineeringShanghai Jiao Tong UniversityShanghai 200030China Shanghai Skin Disease hospital Tongji University School of MedicineShanghai 200092China Shanghai lung {1. Center Shanghai Chest HospitalShanghai Jiao Tong UniversityShanghai 200030China department of Protein Science KTH Royal Institute of TechnologyScience for Life LaboratorySolna 17070Sweden

NDFIP1.has been previously reported as a tumor suppressor in multiple solid tumors,but the function of NDFIP1.in NSCLC and the underlying mechanism are still ***,the WW domain containing proteins can be recognized by NDFIP1.resulted in the loading of the target proteins into ***,whether WW domain-containing transcription regulator 1.WWTR1.also known as TAZ)can be packaged into exosomes by NDFIP1.and if so,whether the release of this oncogenic protein via exosomes has an effect on tumor development has not been investigated to any ***,we first found that NDFIP1.was low expressed in NSCLC samples and cell lines,which is associated with shorter ***,we confirmed the interaction between TAZ and NDFIP1.and the existence of TAZ in exosomes,which requires ***,knockout of NDFIP1.led to TAZ accumulation with no change in its mRNA level and degradation *** the cellular TAZ level could be altered by exosome ***,NDFIP1.inhibited proliferation in vitro and in vivo,and silencing TAZ eliminated the increase of proliferation caused by NDFIP1.***,TAZ was negatively correlated with NDFIP1.in subcutaneous xenograft model and clinical samples,and the serum exosomal TAZ level was lower in NSCLC *** summary,our data uncover a new tumor suppressor,NDFIP1.in NSCLC,and a new exosome-related regulatory mechanism of TAZ.

关键词： NDFIP1 TAZ NSCLC exosome cargo sorting

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Dexamethasone suppresses DU1.5 cell proliferation and cell cycle through inhibition of the extracel{1.lar signal-regulated kinase 1./2 pathway and cyclin D1.expression

引用

Asian Journal of Andrology 2008年第4期10卷 635-641页

作者： qing-Zhen Gao Jia-Ju {1. Zi-Dong liu Hui Zhang Shao-Mei Wang He Xu Friendship Nephrology and Blood Purification Center Jinan City Central Hospital Shandong University School of Medicine Shandong 250013 China department of Urology Shandong Provincial Hospital Shandong 250021 China

Aim： To determine the mechanisms of glucocorticoids in inhibiting advanced prostate {1. growth. Methods： The cell proliferation and cell cycle of prostate {1. DU1.5 cells following dexamethasone treatment were determined by proliferation assay and fluorescence-activated cell sorter. Western blot analysis was carried out to evaluate the effects of dexamethasone on phosphorylation of extracellular signal-regulated kinase （ERK）1.2 and expression of cyclin D1.in DU1.5 cells with or without glucocorticoid receptor （GR） antagonist RU486. Reverse transcription- polymerase chain reaction verified the expression of GR mRNA in DU1.5 cells. Results： Dexamethasone significantly inhibited DU 1.5 cell proliferation at the G0/G1.phase. Westem blot analysis showed a dramatic reduction of ERK1.2 activity and cyclin D1.expression in dexamethasone-treated cells. The decreased phosphorylation of ERK1.2 in dexamethasone-treated cells was attenuated by GR blockade. Additionally, the effects of dexamethasone in inhibiting cyclin D1.expression were altered by GR blockade. Conclusion： Dexamethasone suppresses DU1.5 cell proliferation and cell cycle, and the underlying mechanisms are through the inhibition of phosphorylation of ERK1.2 and cyclin D1.expression. The inhibition of ERK1.2 phosphorylation and cyclin D1.expression is attenuated by GR blockade, suggesting that GR regulates ERK1.2 and cyclin D1.pathways. These observations suggest that dexamethasone has a potential clinical application in prostate {1. therapy.

关键词： dexamethasone prostate cancer extracellular signal-regulated kinase 1.2 cell cycle

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：