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Article ; Online: Retraction Note: HAX-1 Promotes the Chemoresistance, Invasion, and Tumorigenicity of Esophageal Squamous Carcinoma Cells.

Sun, Sa-Jia / Feng, Long / Zhao, Guo-Qiang / Dong, Zi-Ming

2019 Volume 64, Issue 8, Page(s) 2368

Abstract: The Editor-in-Chief has retracted this article [1] because Figure 3c appears to have been modified and reused as Figure 3d. ...

Abstract	The Editor-in-Chief has retracted this article [1] because Figure 3c appears to have been modified and reused as Figure 3d.
Language	English
Publishing date	2019-07-12
Publishing country	United States
Document type	Journal Article ; Retraction of Publication
ZDB-ID	304250-9
ISSN	1573-2568 ; 0163-2116
ISSN (online)	1573-2568
ISSN	0163-2116
DOI	10.1007/s10620-019-05728-x
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Article ; Online: Epigenetic silencing of HIC1 promotes epithelial-mesenchymal transition and drives progression in esophageal squamous cell carcinoma.

Li, Pei / Liu, Xiang / Dong, Zi-Ming / Ling, Zhi-Qiang

Oncotarget

2015 Volume 6, Issue 35, Page(s) 38151–38165

Abstract: Downregulation of the novel tumor suppressor gene HIC1 (hypermethylated in cancer 1) occurs frequently in various tumors where it causes tumor progression and metastasis. In this study, we investigated a role of HIC1 in esophageal squamous cell carcinoma ...

Abstract	Downregulation of the novel tumor suppressor gene HIC1 (hypermethylated in cancer 1) occurs frequently in various tumors where it causes tumor progression and metastasis. In this study, we investigated a role of HIC1 in esophageal squamous cell carcinoma (ESCC) and the underlying mechanisms. Downregulation of HIC1 occurred in approximately 70% of primary ESCCs at both mRNA and protein level where it was associated significantly with vascular invasion, advanced clinical stage, lymph node metastasis, and poor disease free survival (DFS). The promoter methylation analyses suggested that loss of HIC1 expression was mediated by epigenetic mechanisms. Functional studies established that ectopic re-expression of HIC1 in ESCC cells inhibited cell proliferation, clonogenicity, cell motility, tumor formation and epithelial-mesenchymal transition (EMT). Our results decipher the mechanism through which HIC1 deficiency induce ESCC cells to undergo EMT and promote tumor progression and metastasis through activation of EphA2 signaling pathway. Together, loss of the regulation of EphA2 pathway through HIC1 epigenetic silencing could be an important mechanism in the ESCC progression. We identify a novel pathway that linking HIC1 downregulation to EphA2-inducing EMT in ESCC cells and may shed light on the development of novel anti-tumor therapeutics.
MeSH term(s)	Adult ; Aged ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/metabolism ; Carcinoma, Squamous Cell/mortality ; Carcinoma, Squamous Cell/pathology ; Carcinoma, Squamous Cell/therapy ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; DNA Methylation ; Disease Progression ; Down-Regulation ; Epithelial-Mesenchymal Transition ; Esophageal Neoplasms/genetics ; Esophageal Neoplasms/metabolism ; Esophageal Neoplasms/mortality ; Esophageal Neoplasms/pathology ; Esophageal Neoplasms/therapy ; Esophageal Squamous Cell Carcinoma ; Female ; Gene Expression Regulation, Neoplastic ; Gene Silencing ; Humans ; Kaplan-Meier Estimate ; Kruppel-Like Transcription Factors/genetics ; Kruppel-Like Transcription Factors/metabolism ; Male ; Middle Aged ; Neoplasm Invasiveness ; Prognosis ; Promoter Regions, Genetic ; Proportional Hazards Models ; RNA Interference ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Receptor, EphA2/genetics ; Receptor, EphA2/metabolism ; Risk Factors ; Signal Transduction ; Time Factors ; Transcription, Genetic ; Transfection
Chemical Substances	HIC1 protein, human ; Kruppel-Like Transcription Factors ; RNA, Messenger ; Receptor, EphA2 (EC 2.7.10.1)
Language	English
Publishing date	2015-10-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.5832
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Article ; Online: Roles of GST-π and polβ genes in chemoresistance of esophageal carcinoma cells.

Tang, Yue / Xuan, Xiao-Yan / Li, Min / Dong, Zi-Ming

Asian Pacific journal of cancer prevention : APJCP

2014 Volume 14, Issue 12, Page(s) 7375–7379

Abstract: The main aim of this study was to investigate the roles of GST-π and polβ genes in the chemoresistance of esophageal carcinoma cells. Eukaryotic expression vectors containing each gene were constructed and transfected into EC9706 cells, and the ... ...

Abstract	The main aim of this study was to investigate the roles of GST-π and polβ genes in the chemoresistance of esophageal carcinoma cells. Eukaryotic expression vectors containing each gene were constructed and transfected into EC9706 cells, and the biological effects of the two genes assessed based on a resistance index. We additionally investigated the in vitro and in vivo anti-resistance effects of GST-π and polβ genes using recombinant lentiviruses carrying siRNAs against the two genes. Our results showed that upregulation of GST-π and polβ genes suppresses chemosensitivity of esophageal carcinoma cells to cisplatin, while downregulation of these two genes with RNAi technology reverses this chemoresistance. Multi-site injection of recombinant lentivirus targeting the GST-π gene into transplanted cDDP tumors effectively reversed their chemoresistant phenotype. However, the same treatment against the polβ gene did not lead to significant efficacy against chemoresistance.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Blotting, Western ; Cell Proliferation ; Cisplatin/pharmacology ; DNA Polymerase beta/antagonists & inhibitors ; DNA Polymerase beta/genetics ; DNA Polymerase beta/metabolism ; Drug Resistance, Neoplasm/genetics ; Esophageal Neoplasms/drug therapy ; Esophageal Neoplasms/genetics ; Esophageal Neoplasms/pathology ; Flow Cytometry ; Gene Expression Regulation, Neoplastic/drug effects ; Glutathione S-Transferase pi/antagonists & inhibitors ; Glutathione S-Transferase pi/genetics ; Glutathione S-Transferase pi/metabolism ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; RNA, Messenger/genetics ; RNA, Small Interfering/genetics ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays
Chemical Substances	Antineoplastic Agents ; RNA, Messenger ; RNA, Small Interfering ; Glutathione S-Transferase pi (EC 2.5.1.18) ; DNA Polymerase beta (EC 2.7.7.-) ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2014-01-23
Publishing country	Thailand
Document type	Journal Article
ZDB-ID	2218955-5
ISSN	2476-762X ; 1513-7368
ISSN (online)	2476-762X
ISSN	1513-7368
DOI	10.7314/apjcp.2013.14.12.7375
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Article: Epigenetic inactivation of Wnt inhibitory factor-1 in human esophageal squamous cell carcinoma.

Yang, Song-Hua / Li, Sheng-Lei / Dong, Zi-Ming / Kan, Quan-Cheng

Oncology research

2012 Volume 20, Issue 2-3, Page(s) 123–130

Abstract: Wnt inhibitory factor-1 (WIF1), as one of most important Wnt antagonists, has been detected frequently silenced by promoter hypermethylation in various types of cancer. In this study, we aimed to investigate the promoter methylation profiles of WIF1 in ... ...

Abstract	Wnt inhibitory factor-1 (WIF1), as one of most important Wnt antagonists, has been detected frequently silenced by promoter hypermethylation in various types of cancer. In this study, we aimed to investigate the promoter methylation profiles of WIF1 in human esophageal squamous cell carcinoma (ESCC) tissues and cell lines, as well as the functional roles of WIF1 in the human ESCC metastatic behavior. WIF1 mRNA levels and promoter methylation status in ESCC tissues and cell lines were detected using RT-PCR and methylation-specific PCR (MS-PCR), respectively. WIF1 protein levels were assessed by Western blot. Stable ESCC cell line with restoration of WIF1 was generated in EC109 cells, which naturally do not express detectable WIF1 mRNA. The effects of reexpressed WIF1 on EC109 cell proliferation and migration were investigated using crystal violet and wound healing assay, respectively. Also the effects of WIF1 reexpression on the beta-catenin/T-cell factor-dependent transcription activity was measured by luciferase assay. WIF1 promoter methylation was frequently observed in ESCC tissues (46%, 23/50) and cell lines (50%, 2/4). Treatment with demethylating agent, 5-aza-2'-deoxycytidine (5-aza-dC), increased or restored WIF1 expression in these ESCC cell lines. Restoration of the WIF1 in EC109 cells resulted in a significant inhibition on both cell proliferation and migration. Moreover, reexpression of WIF1 caused significant decrease of beta-catenin/T-cell factor-dependent transcription activity. These findings demonstrated that WIF1 silencing due to promoter hypermethylation is a major mechanism during carcinogenesis of ESCC. This would be an opportunity to prevent the development and progression of HCC through modulation of WIF1.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Blotting, Western ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/pathology ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; DNA Methylation ; DNA, Neoplasm/genetics ; Epigenomics ; Esophageal Neoplasms/genetics ; Esophageal Neoplasms/pathology ; Gene Expression Regulation, Neoplastic ; Gene Silencing ; Humans ; Luciferases/metabolism ; Polymerase Chain Reaction ; Promoter Regions, Genetic/genetics ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction ; Repressor Proteins/genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Wound Healing
Chemical Substances	Adaptor Proteins, Signal Transducing ; DNA, Neoplasm ; RNA, Messenger ; Repressor Proteins ; WIF1 protein, human ; Luciferases (EC 1.13.12.-)
Language	English
Publishing date	2012-11-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	1114699-0
ISSN	1555-3906 ; 0965-0407
ISSN (online)	1555-3906
ISSN	0965-0407
DOI	10.3727/096504012x13477145153039
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Article ; Online: HAX-1 promotes the chemoresistance, invasion, and tumorigenicity of esophageal squamous carcinoma cells.

Sun, Sa-jia / Feng, Long / Zhao, Guo-qiang / Dong, Zi-ming

publication RETRACTED

Digestive diseases and sciences

2012 Volume 57, Issue 7, Page(s) 1838–1846

Abstract: Background: HAX-1 is an anti-apoptotic factor and regulates the expression of DNA pol β. Interestingly, DNA polymerase pol β is overexpressed in esophageal squamous cell carcinoma (ESCC). However, the functional role of HAX-1 in ESCC remains unclear.: ...

Abstract	Background: HAX-1 is an anti-apoptotic factor and regulates the expression of DNA pol β. Interestingly, DNA polymerase pol β is overexpressed in esophageal squamous cell carcinoma (ESCC). However, the functional role of HAX-1 in ESCC remains unclear. Aims: To investigate the role of HAX-1 in chemoresistance, invasion, and tumorigenicity of ESCC. Methods: Lentivirus-mediated overexpression or knockdown of HAX-1 was employed to establish ESCC EC9706 cell lines that expressed HAX-1 at different levels. The biological behaviors of these engineered cells were characterized in vitro and in vivo using a xenograft nude mice model. In addition, HAX-1 and pol β expression in the tumor tissues was detected by RT-PCR and immunohistochemistry. Results: HAX-1 overexpression promoted cell proliferation and resistance against cisplatin, increased cell invasion and suppressed apoptosis along with increased pol β expression. Conversely, HAX-1 knockdown inhibited the malignant phenotypes of EC9706 cells. The xenograft nude mice model demonstrated that HAX-1 overexpression or depletion led to increased or decreased tumor growth in vivo, respectively. Furthermore, a positive correlation of HAX-1 and pol β expression in the tumor tissues was observed. Conclusions: HAX-1 promotes the proliferation, chemoresistance, invasion, and tumorigenicity of ESCC, and this is correlated with increased poly β expression. HAX-1 may represent a potential target to overcome the resistance and metastasis of ESCC.
MeSH term(s)	Adaptor Proteins, Signal Transducing/drug effects ; Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/physiology ; Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Carcinoma, Squamous Cell/drug therapy ; Carcinoma, Squamous Cell/pathology ; Carcinoma, Squamous Cell/physiopathology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Cell Survival/physiology ; Cell Transformation, Neoplastic/pathology ; Cisplatin/pharmacology ; Cisplatin/therapeutic use ; Disease Models, Animal ; Drug Resistance, Neoplasm/physiology ; Esophageal Neoplasms/drug therapy ; Esophageal Neoplasms/pathology ; Esophageal Neoplasms/physiopathology ; Female ; HEK293 Cells ; Humans ; In Vitro Techniques ; Mice ; Mice, Nude ; Neoplasm Invasiveness/physiopathology ; RNA, Small Interfering/pharmacology ; Transplantation, Heterologous
Chemical Substances	Adaptor Proteins, Signal Transducing ; Antineoplastic Agents ; HAX1 protein, human ; RNA, Small Interfering ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2012-03-27
Publishing country	United States
Document type	Journal Article ; Retracted Publication
ZDB-ID	304250-9
ISSN	1573-2568 ; 0163-2116
ISSN (online)	1573-2568
ISSN	0163-2116
DOI	10.1007/s10620-012-2108-5
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Article: [Effect of CEA gene regulation on the anti-tumor activity of oncolytic adenovirus H101 to esophageal carcinoma].

Zheng, Hong / Li, Ming-shan / Zhao, Guo-qiang / Dong, Zi-ming

Zhonghua zhong liu za zhi [Chinese journal of oncology

2011 Volume 33, Issue 11, Page(s) 822–826

Abstract: Objective: To study the effect of CEA gene regulation on the anti-tumor activity of oncolytic adenovirus H101 to esophageal carcinoma, and to explore the intrinsic factors influencing H101 sensitivity.: Methods: Stable human esophageal cancer cell ... ...

Abstract	Objective: To study the effect of CEA gene regulation on the anti-tumor activity of oncolytic adenovirus H101 to esophageal carcinoma, and to explore the intrinsic factors influencing H101 sensitivity. Methods: Stable human esophageal cancer cell line EC9706 cells with lower (EC9706-SCEA) and higher CEA expression (EC9706-CEA) were chosen, thawed and cultured, and then to analyse the influence of CEA expressed at different levels on cell growth. The cytotoxic effect of H101 was assayed by in vitro and nude mouse in vivo. Results: The cell growth experiment showed that the population doubling time of EC9706-SCEA, EC9706-CEA and EC9706 cells were (30.9 ± 2.0) h, (31.1 ± 2.5) h and (29.1 ± 2.6) h, respectively, showing no significant difference among them (P > 0.05). The cytotoxic activity of H101 was higher on EC9706-SCEA than on other four groups, when MOI was ≥ 0.01 PFU (P < 0.05). The mouse experiment showed that H101 inhibited the growth of transplanted tumors in all experimental groups. Its effect on CEA-silenced tumors (inhibition rate was 61.5% to 74.5%) was significantly higher than that on CEA-overexpression tumors (32.3% to 38.5%) and control EC9706 transplanted tumors (35.5% to 44.8%). There was a significant difference between them (P < 0.05). Conclusions: The results in vitro and in vivo experiments show that H101 can enhance the cytotoxic effect on EC9706 cells with lower CEA expression. To silence the expression of CEA may provide a novel strategy for target gene therapy of esophageal carcinoma.
MeSH term(s)	Adenoviridae/physiology ; Animals ; Carcinoembryonic Antigen/genetics ; Carcinoembryonic Antigen/metabolism ; Cell Line, Tumor ; Cell Proliferation ; Esophageal Neoplasms/metabolism ; Esophageal Neoplasms/pathology ; Esophageal Neoplasms/therapy ; Female ; Gene Silencing ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Transplantation ; Oncolytic Virotherapy ; Oncolytic Viruses/physiology ; RNA, Messenger/metabolism ; RNA, Small Interfering/genetics ; Tumor Burden
Chemical Substances	Carcinoembryonic Antigen ; RNA, Messenger ; RNA, Small Interfering
Language	Chinese
Publishing date	2011-11
Publishing country	China
Document type	English Abstract ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603424-x
ISSN	0253-3766
ISSN	0253-3766
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Zs.B 2277: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article: [Construction of a siRNA vector targeting human MTA1 gene and the gene-silencing effect].

Yang, Song-hua / Zhao, Guo-qiang / Dong, Zi-ming

Nan fang yi ke da xue xue bao = Journal of Southern Medical University

2008 Volume 28, Issue 3, Page(s) 366–369

Abstract: Objective: To construct an expression vector of siRNA targeting human MTA1 gene and observe its gene-silencing effect in esophageal carcinoma cells.: Methods: The siRNA sequences targeting MTA1 gene were designed and synthesized with two ... ...

Abstract	Objective: To construct an expression vector of siRNA targeting human MTA1 gene and observe its gene-silencing effect in esophageal carcinoma cells. Methods: The siRNA sequences targeting MTA1 gene were designed and synthesized with two complementary oligonucleotide strands. The oligonucleotide strands were annealed and recombined into pRNAT-U6.2 vector, which was identified by sequencing following transformation and amplification. The siRNA expression vector pRNAT-U6.2-MTA1 was transfected into human esophageal carcinoma EC9706 cells via liposome. RT-PCR and Western blotting were used to detect expression levels of MTA1 mRNA and protein in the transfected EC9706 cells, respectively. Results: The double-stranded oligonucleotide fragments of the siRNA targeting MTA1 gene were cloned into pRNAT-U6.2 vector, which was validated by sequence analysis. RT-PCR and Western blotting indicated that MTA1 mRNA and protein expressions were significantly decreased in the transfected cells, especially in those transfected with the siRNA targeting the sequence of GACCCTGCTGGCAGATAAA (481-499), which induced almost complete silencing of MTA1 protein expression. Conclusion: The siRNA expression vector pRNAT-U6.2-MTA1 for silencing MTA1 gene expression in the esophageal carcinoma cells has been successfully constructed, which may facilitate further study for decreasing the invasive and metastatic potentials of malignant tumors by MTA1 gene silencing.
MeSH term(s)	Base Sequence ; Blotting, Western ; Cell Line, Tumor ; Cloning, Molecular ; Esophageal Neoplasms/genetics ; Esophageal Neoplasms/metabolism ; Esophageal Neoplasms/pathology ; Genetic Vectors/genetics ; Histone Deacetylases/biosynthesis ; Histone Deacetylases/genetics ; Humans ; Molecular Sequence Data ; RNA Interference ; RNA, Messenger/biosynthesis ; RNA, Messenger/genetics ; RNA, Small Interfering/genetics ; Repressor Proteins/biosynthesis ; Repressor Proteins/genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Trans-Activators ; Transfection
Chemical Substances	MTA1 protein, human ; RNA, Messenger ; RNA, Small Interfering ; Repressor Proteins ; Trans-Activators ; Histone Deacetylases (EC 3.5.1.98)
Language	Chinese
Publishing date	2008-03-14
Publishing country	China
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2250951-3
ISSN	1673-4254
ISSN	1673-4254
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Article: [Preliminary study of DNA polymerase beta gene silencing by small interfering RNA in human gastric cancer BGC-823 cells].

Zhao, Guo-qiang / Wang, Lei / Dong, Zi-ming

Zhonghua zhong liu za zhi [Chinese journal of oncology

2008 Volume 30, Issue 10, Page(s) 729–732

Abstract: Objective: To study the influence of DNA polymerase beta (polbeta) gene silencing by small interfering RNA on biological behavior of human gastric cancer cell line BGC-823.: Methods: The siRNA eukaryotic expression vectors targeting polbeta gene were ...

Abstract	Objective: To study the influence of DNA polymerase beta (polbeta) gene silencing by small interfering RNA on biological behavior of human gastric cancer cell line BGC-823. Methods: The siRNA eukaryotic expression vectors targeting polbeta gene were constructed and transfected into BGC-823 cells by liposome. Stable cell lines were screened with G418. The expression levels of polbeta mRNA and protein were detected by real time PCR and Western blot in the cells of each group. The proliferation of each group was detected by flow cytometry and tumorigenicity was determined in nude mice. Results: The siRNA expression vector targeting polbeta gene was successfully constructed. The expression levels of polbeta mRNA and protein were significantly reduced in the experimental group transfected with siRNA expression vectors targeting polbeta, and the silencing effect of pRNAT-U6.1-sipolbeta2 (suppression degree was 83%) was stronger than that of pRNAT-U6.1-sipolbeta1 (depression degree is 56%). Compared with irrelevant siRNA control group, empty vector control group and untransfected group, the ratio of G0/G1 cells was increased, proportion of S phase cells and cell proliferation were decreased in the experimental group 1 cells transfected with pRNAT-U6.1-sipolbeta1 (P < 0.05). On the contrary, the ratio of G1/G0 was decreased, proportion of S phase cells and cell proliferation was increased in the experimental group 2 cells transfected with pRNAT-U6.1-sipolbeta2 (P < 0.05). Conclusion: The siRNA expression vectors targeting DNA polymerase beta gene can significantly inhibit the expression of polbeta mRNA. Neither high nor extremely low expression of polbeta is beneficial to maintain the cellular physiological functions. The expression of polbeta silenced to a proper level by siRNA may play an important role in inhibiting tumorigenesis.
MeSH term(s)	Animals ; Cell Cycle ; Cell Line, Tumor ; Cell Proliferation ; DNA Polymerase beta/genetics ; DNA Polymerase beta/metabolism ; Gene Silencing ; Genetic Vectors ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Transplantation ; RNA, Messenger/metabolism ; RNA, Small Interfering ; Random Allocation ; Stomach Neoplasms/metabolism ; Stomach Neoplasms/pathology ; Transfection ; Tumor Burden
Chemical Substances	RNA, Messenger ; RNA, Small Interfering ; DNA Polymerase beta (EC 2.7.7.-)
Language	Chinese
Publishing date	2008-10
Publishing country	China
Document type	English Abstract ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603424-x
ISSN	0253-3766
ISSN	0253-3766
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Article ; Online: Down-regulation of PTEN expression modulated by dysregulated miR-21 contributes to the progression of esophageal cancer.

Li, Pei / Mao, Wei-Min / Zheng, Zhi-Guo / Dong, Zi-Ming / Ling, Zhi-Qiang

Digestive diseases and sciences

2013 Volume 58, Issue 12, Page(s) 3483–3493

Abstract: Background and aim: miR-21, a putative tumor oncomiR, is a frequently overexpressed miRNA in a variety of tumors. Because it targets tumor-suppressor genes it has been linked to tumor progression. In this study we investigated the role of miR-21 in ... ...

Abstract	Background and aim: miR-21, a putative tumor oncomiR, is a frequently overexpressed miRNA in a variety of tumors. Because it targets tumor-suppressor genes it has been linked to tumor progression. In this study we investigated the role of miR-21 in esophageal squamous cell carcinoma (ESCC), and its possible mechanism. Methods: Expression of miR-21 was detected by stem-loop RT-PCR in tissue from 76 invasive ESCC at stage I-IV and in their corresponding para-cancerous histological normal tissues (PCHNT). Thirty endoscopic esophageal mucosal biopsy specimens from non-tumor patients were used as controls. Expression of PTEN in 76 paired ESCC and PCHNT was investigated by real-time RT-PCR and an immunohistochemical method, respectively. Paired tumor and PCHNT specimens of 20 ESCC cases were randomly selected for western blot analysis. The effect of miR-21 on PTEN expression was assessed in the ESCC cell line with an miR-21 inhibitor to reduce miR-21 expression. Furthermore, the roles of miR-21 in cell biology were analyzed by use of miR-21 inhibitor-transfected cells. Results: Stem-loop RT-PCR revealed miR-21 was significantly overexpressed in ESCC tissues and cell lines. Overexpression of miR-21 correlated with tumor status, lymph node metastasis, and clinical stage. We demonstrated that knockdown of miR-21 significantly increased expression of PTEN protein. Consequent PTEN expression reduced cell proliferation, invasion, and migration. Conclusions: Our findings suggest that miR-21 could be a potential oncomiR, probably by regulation of PTEN, and a novel prognostic factor for ESCC patients.
MeSH term(s)	Adult ; Aged ; Biomarkers, Tumor/metabolism ; Carcinoma, Squamous Cell/metabolism ; Carcinoma, Squamous Cell/mortality ; Carcinoma, Squamous Cell/pathology ; Cell Line, Tumor ; China/epidemiology ; Disease Progression ; Down-Regulation ; Esophageal Neoplasms/metabolism ; Esophageal Neoplasms/mortality ; Esophageal Neoplasms/pathology ; Esophagus/pathology ; Female ; Humans ; Male ; MicroRNAs/physiology ; Middle Aged ; PTEN Phosphohydrolase/antagonists & inhibitors ; PTEN Phosphohydrolase/biosynthesis ; Up-Regulation
Chemical Substances	Biomarkers, Tumor ; MIRN21 microRNA, human ; MicroRNAs ; PTEN Phosphohydrolase (EC 3.1.3.67) ; PTEN protein, human (EC 3.1.3.67)
Language	English
Publishing date	2013-09-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	304250-9
ISSN	1573-2568 ; 0163-2116
ISSN (online)	1573-2568
ISSN	0163-2116
DOI	10.1007/s10620-013-2854-z
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Article: DNA polymerase beta overexpression correlates with poor prognosis in esophageal cancer patients

Zheng, Hong / Xue, Peng / Li, Min / Zhao, JiMin / Dong, ZiMing / Zhao, GuoQiang

Chinese science bulletin Kexue tongbao.. 2013 Sept., v. 58, no. 26

2013

Abstract: Gene of DNA polymerase beta (polβ) plays an important role in base excision repair, DNA replication and translesion synthesis. This study aims to investigate the expression and prognostic significance of DNA polβ in esophageal cancer. DNA polβ expression ...

Abstract	Gene of DNA polymerase beta (polβ) plays an important role in base excision repair, DNA replication and translesion synthesis. This study aims to investigate the expression and prognostic significance of DNA polβ in esophageal cancer. DNA polβ expression was analyzed using real-time quantitative PCR (RT-qPCR) and immunohistochemical staining on tissue samples from a consecutive series of 114 esophageal squamous carcinoma patients who underwent resections between 2002 and 2006. Polβ expression was investigated on its correlation to clinico-pathological factors and survival. RT-qPCR results showed higher expression of DNA polβ mRNA in tumor tissue than in its matched adjacent non-tumor tissue sample, different expression of DNA polβ mRNA was noticed with significance between tumors with and without lymph node metastasis. Immunohistochemistry staining results indicated the polβ strong-positive rate was 44.73% (51/114) in tumor tissue samples and 0.00% in matched adjacent non-tumor tissue samples, with significant difference. Kaplan-Meier survival curves revealed that high expression of pol? was associated with tumor metastasis and poor prognosis in esophageal cancer patients. Our data suggests that polβ plays an important role in tumor progression and that high polβ expression predicts an unfavorable prognosis in esophageal squamous carcinoma patients.
Keywords	DNA ; DNA repair ; DNA replication ; DNA-directed DNA polymerase ; carcinoma ; esophageal neoplasms ; gene overexpression ; genes ; immunohistochemistry ; lymph ; messenger RNA ; metastasis ; patients ; prognosis ; quantitative polymerase chain reaction
Language	English
Dates of publication	2013-09
Size	p. 3274-3279.
Publishing place	Springer-Verlag
Document type	Article
ZDB-ID	1021576-1
ISSN	1861-9541 ; 1001-6538 ; 0250-7862
ISSN (online)	1861-9541
ISSN	1001-6538 ; 0250-7862
DOI	10.1007/s11434-013-5956-2
Database	NAL-Catalogue (AGRICOLA)

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