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Article: miR-622 Increases miR-30a Expression through Inhibition of Hypoxia-Inducible Factor 1α to Improve Metastasis and Chemoresistance in Human Invasive Breast Cancer Cells.

Cheng, Chun-Wen / Liu, Yu-Fan / Liao, Wen-Ling / Chen, Po-Ming / Hung, Yueh-Tzu / Lee, Huei-Jane / Cheng, Yu-Chun / Wu, Pei-Ei / Lu, Yen-Shen / Shen, Chen-Yang

Cancers

2024 Volume 16, Issue 3

Abstract: Hypoxia-inducible factor 1α (HIF-1α) plays a pivotal role in the survival, metastasis, and response to treatment of solid tumors. Autophagy serves as a mechanism for tumor cells to eliminate misfolded proteins and damaged organelles, thus promoting ... ...

Abstract	Hypoxia-inducible factor 1α (HIF-1α) plays a pivotal role in the survival, metastasis, and response to treatment of solid tumors. Autophagy serves as a mechanism for tumor cells to eliminate misfolded proteins and damaged organelles, thus promoting invasiveness, metastasis, and resistance to treatment under hypoxic conditions. MicroRNA (miRNA) research underscores the significance of these non-coding molecules in regulating cancer-related protein synthesis across diverse contexts. However, there is limited reporting on miRNA-mediated gene expression studies, especially with respect to epithelial-mesenchymal transition (EMT) and autophagy in the context of hypoxic breast cancer. Our study reveals decreased levels of miRNA-622 (miR-622) and miRNA-30a (miR-30a) in invasive breast cancer cells compared to their non-invasive counterparts. Inducing miR-622 suppresses HIF-1α protein expression, subsequently activating miR-30a transcription. This cascade results in reduced invasiveness and migration of breast cancer cells by inhibiting EMT markers, such as Snail, Slug, and vimentin. Furthermore, miR-30a negatively regulates beclin 1, ATG5, and LC3-II and inhibits Akt protein phosphorylation. Consequently, this improves the sensitivity of invasive MDA-MB-231 cells to docetaxel treatment. In conclusion, our study highlights the therapeutic potential of inducing miR-622 to promote miR-30a expression and thus disrupt HIF-1α-associated EMT and autophagy pathways. This innovative strategy presents a promising approach to the treatment of aggressive breast cancer.
Language	English
Publishing date	2024-02-03
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers16030657
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Article ; Online: 'Hide-then-hit' to explain the importance of genotypic polymorphism of DNA repair genes in determining susceptibility to cancer.

Wu, Pei-Ei / Shen, Chen-Yang

Journal of molecular cell biology

2011 Volume 3, Issue 1, Page(s) 59–65

Abstract: Interindividual variations in DNA repair capacity/efficiency linked to the presence of polymorphisms in DNA repair-related genes have been suggested to account for different risk of developing cancers. In this review article, on the basis of breast ... ...

Abstract	Interindividual variations in DNA repair capacity/efficiency linked to the presence of polymorphisms in DNA repair-related genes have been suggested to account for different risk of developing cancers. In this review article, on the basis of breast cancer formation as a model, we propose a 'hide-then-hit' hypothesis indicating the importance of escaping checkpoint surveillance for sub-optimal DNA repair variants to cause cancer. Therefore, only cells with subtle defects in repair capacity arising from low-penetrance variants of DNA repair genes would have the opportunity to grow and accumulate the genetic changes needed for cancer formation, without triggering cell-cycle checkpoint surveillance. Furthermore, distinct from high-penetrance alleles, these polymorphic alleles of DNA repair genes would predispose carriers to a higher risk of developing cancer but would not necessarily cause cancer. To examine this, we simultaneously genotyped multiple SNPs of cell-cycle checkpoint genes and the DNA repair genes. Support for the hypothesis came from observations that breast cancer risk associated with variant genotypes of DNA repair genes became more significant in the subgroups of women with specific genotypic statuses of checkpoint genes. This 'hide-then-hit' hypothesis is certainly needed to be confirmed by biological evidence in which a cause-effect relationship has to be established. However, based on this, possible gene-gene interaction is considered to play an important role in modifying the cancer risk associated with genotypic polymorphism of DNA repair gene in different study populations.
MeSH term(s)	DNA Repair/genetics ; Genetic Predisposition to Disease/genetics ; Genotype ; Humans ; Neoplasms/genetics ; Polymorphism, Genetic
Language	English
Publishing date	2011-02
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2500949-7
ISSN	1759-4685 ; 1674-2788
ISSN (online)	1759-4685
ISSN	1674-2788
DOI	10.1093/jmcb/mjq054
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Article ; Online: Blood multiomics reveal insights into population clusters with low prevalence of diabetes, dyslipidemia and hypertension.

Su, Ming-Wei / Chang, Chung-Ke / Lin, Chien-Wei / Ling, Shiu-Jie / Hsiung, Chia-Ni / Chu, Hou-Wei / Wu, Pei-Ei / Shen, Chen-Yang

PloS one

2020 Volume 15, Issue 3, Page(s) e0229922

Abstract: Diabetes, dyslipidemia and hypertension are important metabolic diseases that impose a great burden on many populations worldwide. However, certain population strata have reduced prevalence for all three diseases, but the underlying mechanisms are poorly ...

Abstract	Diabetes, dyslipidemia and hypertension are important metabolic diseases that impose a great burden on many populations worldwide. However, certain population strata have reduced prevalence for all three diseases, but the underlying mechanisms are poorly understood. We sought to identify the phenotypic, genomic and metabolomic characteristics of the low-prevalence population to gain insights into possible innate non-susceptibility against metabolic diseases. We performed k-means cluster analysis of 16,792 subjects using anthropometric and clinical biochemistry data collected by the Taiwan Biobank. Nuclear magnetic resonance spectra-based metabolome analysis was carried out for 217 subjects with normal body mass index, good exercise habits and healthy lifestyles. We found that the gene APOA5 was significantly associated with reduced prevalence of disease, and lesser associations included the genes HIF1A, LIMA1, LPL, MLXIPL, and TRPC4. Blood plasma of subjects belonging to the low disease prevalence cluster exhibited lowered levels of the GlycA inflammation marker, very low-density lipoprotein and low-density lipoprotein cholesterol, triglycerides, valine and leucine compared to controls. Literature mining revealed that these genes and metabolites are biochemically linked, with the linkage between lipoprotein metabolism and inflammation being particularly prominent. The combination of phenomic, genomic and metabolomic analysis may also be applied towards the study of metabolic disease prevalence in other populations.
MeSH term(s)	Adult ; Cholesterol, LDL/blood ; Cluster Analysis ; Cohort Studies ; Diabetes Mellitus/blood ; Diabetes Mellitus/epidemiology ; Dyslipidemias/blood ; Dyslipidemias/epidemiology ; Female ; Genome-Wide Association Study ; Genotype ; Healthy Volunteers ; Humans ; Hypertension/blood ; Hypertension/epidemiology ; Male ; Metabolome ; Middle Aged ; Phenotype ; Polymorphism, Single Nucleotide ; Prevalence ; Taiwan/epidemiology
Chemical Substances	Cholesterol, LDL
Language	English
Publishing date	2020-03-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0229922
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Article: MiR-139 Modulates Cancer Stem Cell Function of Human Breast Cancer through Targeting CXCR4.

Cheng, Chun-Wen / Liao, Wen-Ling / Chen, Po-Ming / Yu, Jyh-Cherng / Shiau, Hui-Ping / Hsieh, Yi-Hsien / Lee, Huei-Jane / Cheng, Yu-Chun / Wu, Pei-Ei / Shen, Chen-Yang

Cancers

2021 Volume 13, Issue 11

Abstract: Elevated expression of C-X-C motif chemokine receptor 4 (CXCR4) correlates with chemotaxis, invasion, and cancer stem cell (CSC) properties within several solid-tumor malignancies. Recent studies reported that microRNA (miRNA) modulates the stemness of ... ...

Abstract	Elevated expression of C-X-C motif chemokine receptor 4 (CXCR4) correlates with chemotaxis, invasion, and cancer stem cell (CSC) properties within several solid-tumor malignancies. Recent studies reported that microRNA (miRNA) modulates the stemness of embryonic stem cells. We aimed to investigate the role of miRNA, via CXCR4-modulation, on CSC properties in breast cancer using cell lines and xenotransplantation mouse model and evaluated miR-193 levels in 191 patients with invasive ductal carcinoma. We validated miR-139 directly targets the 3'-untranslated region of CXCR4. Hoechst 33342 fluorescence-activated cell sorting (FACS) and sphere-forming assay were used to identify CSCs. MiR-139 suppressed breast CSCs with mesenchymal traits; led to decreased migration and invasion abilities through down-regulating CXCR4/p-Akt signaling. In lung cancer xenograft model of nude mice transplanted with human miR-139-carrying MDA-MB-231 cells, metastatic lung nodules were suppressed. Clinically, microdissected breast tumor tissues showed miR-139 reduction, compared to adjacent non-tumor tissues, that was significantly associated with worse clinicopathological features, including larger tumor size, advanced tumor stage and lymph node metastasis; moreover, reduced miR-139 level was predominately occurred in late-stage HER2-oreexpression tumors. Collectively, our findings highlight miR-139-mediated suppression of CXCR4/p-Akt signaling and thereby affected mesenchymal stem-cell genesis, indicating its potential as a therapeutic target for invasive breast cancer.
Language	English
Publishing date	2021-05-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13112582
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Article ; Online: A high-resolution HLA imputation system for the Taiwanese population: a study of the Taiwan Biobank.

Huang, Yu-Han / Khor, Seik-Soon / Zheng, Xiuwen / Chen, Hsuan-Yu / Chang, Ya-Hsuan / Chu, Hou-Wei / Wu, Pei-Ei / Lin, Yu-Ju / Liao, Shu-Fen / Shen, Chen-Yang / Tokunaga, Katsushi / Lee, Mei-Hsuan

The pharmacogenomics journal

2020 Volume 20, Issue 5, Page(s) 695–704

Abstract: An imputation algorithm for human leukocyte antigen (HLA) is helpful for exploring novel disease associations. However, population-specific HLA imputation references are essential for achieving high imputation accuracy. In this study, a subset of 1012 ... ...

Abstract	An imputation algorithm for human leukocyte antigen (HLA) is helpful for exploring novel disease associations. However, population-specific HLA imputation references are essential for achieving high imputation accuracy. In this study, a subset of 1012 individuals from the Taiwan Biobank (TWB) who underwent both whole-genome SNP array and NGS-based HLA typing were used to establish Taiwanese HLA imputation references. The HIBAG package was used to generate the imputation references for eight HLA loci at a two- and three-field resolution. Internal validation was carried out to evaluate the call threshold and accuracy for each HLA gene. HLA class II genes found to be associated with rheumatoid arthritis (RA) were validated in this study by the imputed HLA alleles. Our Taiwanese population-specific references achieved average HLA imputation accuracies of 98.11% for two-field and 98.08% for three-field resolution. The frequency distribution of imputed HLA alleles among 23,972 TWB subjects were comparable with PCR-based HLA alleles in general Taiwanese reported in the allele frequency net database. We replicated four common HLA alleles (HLA-DRB103:01, DRB104:05, DQA103:03, and DQB104:01) significantly associated with RA. The population-specific references provide an informative tool to investigate the associations of HLA variants and human diseases in large-scale population-based studies.
MeSH term(s)	Arthritis, Rheumatoid/diagnosis ; Arthritis, Rheumatoid/genetics ; Arthritis, Rheumatoid/immunology ; Databases, Genetic ; Genetics, Population ; Genotype ; HLA Antigens/genetics ; HLA-DQ alpha-Chains/genetics ; HLA-DQ beta-Chains/genetics ; HLA-DRB1 Chains/genetics ; High-Throughput Nucleotide Sequencing ; Humans ; Phenotype ; Polymorphism, Single Nucleotide ; Reproducibility of Results ; Taiwan ; Whole Genome Sequencing
Chemical Substances	HLA Antigens ; HLA-DQ alpha-Chains ; HLA-DQ beta-Chains ; HLA-DQA1 antigen ; HLA-DQB1 antigen ; HLA-DRB1 Chains ; HLA-DRB103:01 antigen ; HLA-DRB104:05 antigen
Language	English
Publishing date	2020-02-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Validation Study
ZDB-ID	2106831-8
ISSN	1473-1150 ; 1470-269X
ISSN (online)	1473-1150
ISSN	1470-269X
DOI	10.1038/s41397-020-0156-3
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Zs.A 5806: Show issues

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Article ; Online: The Causal Relationship of Circulating Triglyceride and Glycated Hemoglobin: A Mendelian Randomization Study.

Hsiung, Chia-Ni / Chang, Yi-Cheng / Lin, Chien-Wei / Chang, Chia-Wei / Chou, Wen-Cheng / Chu, Hou-Wei / Su, Ming-Wei / Wu, Pei-Ei / Shen, Chen-Yang

The Journal of clinical endocrinology and metabolism

2019 Volume 105, Issue 3

Abstract: Context: The association between circulating triglyceride (TG) and glycated hemoglobin A1c (HbA1c), a biomarker for type 2 diabetes, has been widely addressed, but the causal direction of the relationship is still ambiguous.: Objective: To confirm ... ...

Abstract	Context: The association between circulating triglyceride (TG) and glycated hemoglobin A1c (HbA1c), a biomarker for type 2 diabetes, has been widely addressed, but the causal direction of the relationship is still ambiguous. Objective: To confirm the causal relationship between TG and HbA1c by using bidirectional and 2-step Mendelian randomization (MR) approaches. Methods: We carried out a bidirectional MR approach using the summarized results from the public database to examine any potential causal effects between serum TG and HbA1c in 16 000 individuals of the Taiwan Biobank cohort. We used the MR estimate and the MR inverse variance-weighted method to reveal that relationship between TG and HbA1c. To further determine whether the DNA methylation at specific sequences mediate the causal pathway between TG and HbA1c, using the 2-step MR approach. Results: We identified that a single-unit increase in TG measured via log transformation of mg/dL data was associated with a significant increase of 10 units of HbA1c (95% CI = 1.05-18.95, P = 0.029). In contrast, the genetic determinants of HbA1c do not contribute to the amount of circulating TG (beta = 1.75, 95% CI = -11.50 to 14.90). Sensitivity analyses, included the weighted-median approach and MR-Egger regression, were performed to confirm no pleiotropic effect among these instrumental variables. Furthermore, we identified the genetic variant, rs1823200, is associated with both methylation of the CpG site adjacent to CADPS gene and HbA1c level. Conclusion: Our study suggests that higher circulating TG can have an affect on genomic methylation status, ultimately causing elevated level of circulating HbA1c.
MeSH term(s)	Adult ; Biological Specimen Banks ; Calcium-Binding Proteins/blood ; CpG Islands ; DNA Methylation ; Diabetes Mellitus, Type 2/blood ; Diabetes Mellitus, Type 2/genetics ; Female ; Genetic Predisposition to Disease ; Genetic Variation ; Glycated Hemoglobin A/genetics ; Humans ; Hyperlipidemias/blood ; Hyperlipidemias/genetics ; Male ; Mendelian Randomization Analysis ; Middle Aged ; Regression Analysis ; Taiwan ; Triglycerides/blood ; Triglycerides/genetics ; Vesicular Transport Proteins/blood
Chemical Substances	CADPS protein, human ; Calcium-Binding Proteins ; Glycated Hemoglobin A ; Triglycerides ; Vesicular Transport Proteins ; hemoglobin A1c protein, human
Language	English
Publishing date	2019-11-29
Publishing country	United States
Document type	Evaluation Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/clinem/dgz243
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Article: Body mass index and type 2 diabetes and breast cancer survival: a Mendelian randomization study.

American journal of cancer research

2021 Volume 11, Issue 8, Page(s) 3921–3934

Abstract: The causal relationship between body mass index (BMI) and type 2 diabetes (T2D) and breast cancer prognosis is still ambiguous. The aim of this study was to investigate the prognostic effect of BMI and T2D on breast cancer disease-free survival (DFS) ... ...

Abstract	The causal relationship between body mass index (BMI) and type 2 diabetes (T2D) and breast cancer prognosis is still ambiguous. The aim of this study was to investigate the prognostic effect of BMI and T2D on breast cancer disease-free survival (DFS) among Asian individuals. In this two-sample Mendelian randomization (MR) study, the instrumental variables (IVs) were identified using a genome-wide association study (GWAS) among 24,000 participants in the Taiwan Biobank. Importantly, the validity of these IVs was confirmed with a previous large-scale GWAS (Biobank Japan Project, BBJ). In this study, we found that a genetic predisposition toward higher BMI (as indicated by BMI IVs, F = 86.88) was associated with poor breast cancer DFS (hazard ratio [HR] = 6.11; P < 0.001). Furthermore, higher level of genetically predicted T2D (as indicated by T2D IVs) was associated with an increased risk of recurrence of and mortality from breast cancer (HR = 1.43; P < 0.001). Sensitivity analyses, including the weighted-median approach, MR-Egger regression, Radial regression and Mendelian randomization pleiotropy residual sum and outlier (MR-PRESSO) supported the consistency of our findings. Finally, the causal relationship between BMI and poor breast cancer prognosis was confirmed in a prospective cohort study. Our MR analyses demonstrated the causal relationship between the genetic prediction of elevated BMI and a greater risk of T2D with poor breast cancer prognosis. BMI and T2D have important clinical implications and may be used as prognostic indicators of breast cancer.
Language	English
Publishing date	2021-08-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2589522-9
ISSN	2156-6976
ISSN	2156-6976
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Article ; Online: Genetic Evidence for the Association between Schizophrenia and Breast Cancer.

Shi, Jiajun / Wu, Lang / Zheng, Wei / Wen, Wanqing / Wang, Shuyang / Shu, Xiang / Long, Jirong / Shen, Chen-Yang / Wu, Pei-Ei / Saloustros, Emmanouil / Chang-Claude, Jenny / Brenner, Hermann / Shu, Xiao-Ou / Cai, Qiuyin

Journal of psychiatry and brain science

2018 Volume 3, Issue 4

Abstract: Objective: To estimate the potential effect of schizophrenia on breast cancer risk in women, we performed a two-sample Mendelian randomization (MR) study.: Methods: The instrumental variables comprised 170 uncorrelated and non-pleiotropic single ... ...

Abstract	Objective: To estimate the potential effect of schizophrenia on breast cancer risk in women, we performed a two-sample Mendelian randomization (MR) study. Methods: The instrumental variables comprised 170 uncorrelated and non-pleiotropic single nucleotide polymorphisms (SNPs) that are significantly associated with schizophrenia risk in genome-wide association studies in 105,000 European descent individuals of the Psychiatric Genomics Consortium (http://www.med.unc.edu/pgc/) and the United Kingdom Clozapine Clinic. The association between these SNPs determined schizophrenia and breast cancer risk was estimated in approximately 229,000 European descent females from the Breast Cancer Association Consortium using the inverse-variance weighted and the weighted median MR methods. Results: We found that the genetically-predicted risk of schizophrenia was associated with increased breast cancer risk (under a random-effects model: odds ratio per 1 unit increase in log odds of schizophrenia = 1.04, 95% confidence interval: 1.02-1.06, Conclusion: Our findings implicate a modest increased risk for breast cancer in genetically determined schizophrenic females.
Language	English
Publishing date	2018-08-08
Publishing country	England
Document type	Journal Article
ISSN	2398-385X
ISSN (online)	2398-385X
DOI	10.20900/jpbs.20180007
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Article ; Online: Increased Cellular Levels of MicroRNA-9 and MicroRNA-221 Correlate with Cancer Stemness and Predict Poor Outcome in Human Breast Cancer.

Cheng, Chun-Wen / Yu, Jyh-Cherng / Hsieh, Yi-Hsien / Liao, Wen-Ling / Shieh, Jia-Ching / Yao, Chung-Chin / Lee, Huei-Jane / Chen, Po-Ming / Wu, Pei-Ei / Shen, Chen-Yang

Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

2018 Volume 48, Issue 5, Page(s) 2205–2218

Abstract: Background /Aims: Recent studies of microRNA (miRNA) involvement in tumorigenesis have indicated the critical role of these non-coding small RNAs in malignant transformation, but the prognostic role, if any, of miRNAs in breast cancer remains ... ...

Abstract	Background /Aims: Recent studies of microRNA (miRNA) involvement in tumorigenesis have indicated the critical role of these non-coding small RNAs in malignant transformation, but the prognostic role, if any, of miRNAs in breast cancer remains undetermined. Therefore, we assessed the prognostic significance of microRNA-9 (miR-9) and miR-221 in breast cancer toward the goal of understanding the contribution(s) of these miRNAs to cancer cell stemness. Methods: The level of each of miR-9 and miR-221 in 206 paired laser capture microdissected tumor cells and non-tumor cells was determined by quantitative reverse transcription-PCR (qRT-PCR). The relationship between the miRNA signature and clinicopathological data and prognosis of breast cancer was assessed. Identification of a stem cell-enriched side population was achieved with fluorescence-activated cell sorting and a sphere-forming assay. Wound healing, Boyden chamber assays, and western blotting were used to study the contribution of each miRNA to tumor cell migration and invasion. Results: We found that induction of miR-9 and miR-221 mimics conferred side-population cells to form spheroidal tumor colonies in suspension culture that maintained the mesenchymal stem-cell potential in non-invasive MCF-7 breast cancer cells. In contrast, knockdown of both miR-9 and miR-221 in invasive MDA-MB-231 breast cancer cells dramatically decreased the number of side-population colonies with stem cell-like potency, which reduced the capacity for tumor-cell renewal, invasion, and migration. Clinically, the mean proportion of miR-9- or miR-221-overexpressing cells was significantly greater in tumor cells compared with non-tumor cells (P < 0.05). Increased levels of miR-9 and miR-221 in breast tissue portended a significantly elevated risk of progression to malignancy with respect to larger tumor size, poor differentiation, late-stage evolution, lymph-node metastasis (P < 0.05), and lower overall survival (Ptrend = 0.017; eight-year follow-up). Conclusion: Our findings provide strong evidence that miR-9 and miR-221 can enhance the generation of cancer stem cells to yield an invasive phenotype and that overexpression of these miRNAs predicts a poor outcome for breast cancer patients.
MeSH term(s)	AC133 Antigen/metabolism ; Adult ; Antagomirs/metabolism ; Area Under Curve ; Breast Neoplasms/diagnosis ; Breast Neoplasms/genetics ; Breast Neoplasms/mortality ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Cell Movement ; Female ; Humans ; Lymphatic Metastasis ; MCF-7 Cells ; MicroRNAs/antagonists & inhibitors ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Middle Aged ; Nanog Homeobox Protein/metabolism ; Neoplastic Stem Cells/cytology ; Neoplastic Stem Cells/metabolism ; Prognosis ; Proportional Hazards Models ; ROC Curve ; Survival Rate
Chemical Substances	AC133 Antigen ; Antagomirs ; MIRN221 microRNA, human ; MIRN92 microRNA, human ; MicroRNAs ; Nanog Homeobox Protein
Language	English
Publishing date	2018-08-15
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1067572-3
ISSN	1421-9778 ; 1015-8987
ISSN (online)	1421-9778
ISSN	1015-8987
DOI	10.1159/000492561
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Zs.A 3160: Show issues

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Article ; Online: SUMOylation of XRCC1 activated by poly (ADP-ribosyl)ation regulates DNA repair.

Hu, Ling-Yueh / Chang, Che-Chang / Huang, Yen-Sung / Chou, Wen-Cheng / Lin, Ying-Mei / Ho, Chun-Chen / Chen, Wei-Ting / Shih, Hsiu-Ming / Hsiung, Chia-Ni / Wu, Pei-Ei / Shen, Chen-Yang

Human molecular genetics

2018 Volume 27, Issue 13, Page(s) 2306–2317

Abstract: XRCC1 is an essential scaffold protein for base excision repair (BER) and helps to maintain genomic stability. XRCC1 has been indicated as a substrate for small ubiquitin-like modifier modification (SUMOylation); however, how XRCC1 SUMOylation is ... ...

Abstract	XRCC1 is an essential scaffold protein for base excision repair (BER) and helps to maintain genomic stability. XRCC1 has been indicated as a substrate for small ubiquitin-like modifier modification (SUMOylation); however, how XRCC1 SUMOylation is regulated in cells and how SUMOylated XRCC1 regulates BER activity are not well understood. Here, we show that SUMOylation of XRCC1 is regulated in cells under methyl-methanesulfonate (MMS) treatment and facilitates BER. Poly(ADP-ribose) polymerase 1 (PARP1) is activated by MMS immediately and synthesizes poly(ADP-ribose) (PAR), which in turn promotes recruitment of SUMO E3 TOPORS to XRCC1 and facilitates XRCC1 SUMOylation. A SUMOylation-defective mutant of XRCC1 had lower binding activity for DNA polymerase beta (POLB) and was linked to a lower capacity for repair of MMS-induced DNA damages. Our study therefore identified a pathway in which DNA damage-induced poly(ADP-ribosyl)ation (PARylation) promotes SUMOylation of XRCC1, which leads to more efficient recruitment of POLB to complete BER.
MeSH term(s)	Alcohol Oxidoreductases/genetics ; DNA Damage/drug effects ; DNA Polymerase beta/genetics ; DNA Repair/genetics ; DNA-Binding Proteins/genetics ; Genomic Instability/genetics ; Humans ; Methyl Methanesulfonate/pharmacology ; Poly (ADP-Ribose) Polymerase-1/genetics ; Poly ADP Ribosylation/genetics ; Protein Binding/genetics ; Sumoylation/genetics ; X-ray Repair Cross Complementing Protein 1/genetics
Chemical Substances	DNA-Binding Proteins ; X-ray Repair Cross Complementing Protein 1 ; Methyl Methanesulfonate (AT5C31J09G) ; Alcohol Oxidoreductases (EC 1.1.-) ; phenylacetaldehyde reductase (EC 1.1.1-) ; Poly (ADP-Ribose) Polymerase-1 (EC 2.4.2.30) ; DNA Polymerase beta (EC 2.7.7.-) ; POLB protein, human (EC 2.7.7.7)
Language	English
Publishing date	2018-04-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1108742-0
ISSN	1460-2083 ; 0964-6906
ISSN (online)	1460-2083
ISSN	0964-6906
DOI	10.1093/hmg/ddy135
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