11 results on '"Fangfeng Liu"'
Search Results
2. Interaction Between Polymorphisms of IFN-γ and MICA Correlated with Hepatocellular Carcinoma
- Author
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Jun Lu, Fangfeng Liu, Xu Zhou, Hongguang Li, Jin-Hua Hu, Hong Chang, and Huaqiang Zhu
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Male ,0301 basic medicine ,medicine.medical_specialty ,Carcinoma, Hepatocellular ,Single-nucleotide polymorphism ,Biology ,Polymorphism, Single Nucleotide ,Gastroenterology ,Interferon-gamma ,03 medical and health sciences ,0302 clinical medicine ,Gene Frequency ,Clinical Research ,Internal medicine ,Genotype ,medicine ,Carcinoma ,Humans ,SNP ,Genetic Predisposition to Disease ,Gene ,Genetic Association Studies ,Polymorphism, Genetic ,Histocompatibility Antigens Class I ,Liver Neoplasms ,Epistasis, Genetic ,General Medicine ,Odds ratio ,Middle Aged ,medicine.disease ,digestive system diseases ,Confidence interval ,030104 developmental biology ,030220 oncology & carcinogenesis ,Hepatocellular carcinoma ,Cancer research ,Female ,Interferons - Abstract
BACKGROUND We explored the relationship of interferon-γ (IFN-γ) and MHC class-I chain related gene A (MICA) genes polymorphisms with hepatocellular carcinoma (HCC) risk, and tried to determine whether the interaction existed between these two genes polymorphisms on the basis of HCC. MATERIAL AND METHODS Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method was used to detect the genotypes of the 3 single-nucleotide polymorphisms (SNPs) and to analyze the correlation of each SNP with HCC susceptibility in 120 HCC patients and 124 healthy people. The association strength between the 3 SNPs and HCC is represented with odds ratio (OR) and 95% confidence interval (95% CI). Hardy-Weinberg equilibrium (HWE) was tested by χ2 test in the control group. RESULTS GG genotype of IFN-γ rs2069727 polymorphism had apparently different distributions in case and control groups (P
- Published
- 2016
3. Insulin-like growth factor-1 induces epithelial-mesenchymal transition in hepatocellular carcinoma by activating survivin
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Fangfeng Liu, Hongguang Li, Hengjun Gao, Hong Chang, Yongjie Sun, Jun Lu, Huaqiang Zhu, Xu Zhou, and Bingqi Liu
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0301 basic medicine ,Cancer Research ,Small interfering RNA ,Carcinoma, Hepatocellular ,Epithelial-Mesenchymal Transition ,Survivin ,Down-Regulation ,Vimentin ,Inhibitor of apoptosis ,Inhibitor of Apoptosis Proteins ,03 medical and health sciences ,0302 clinical medicine ,Downregulation and upregulation ,Cell Movement ,Humans ,Gene silencing ,Neoplasm Invasiveness ,RNA, Messenger ,Epithelial–mesenchymal transition ,Insulin-Like Growth Factor I ,RNA, Small Interfering ,neoplasms ,biology ,Liver Neoplasms ,General Medicine ,Cell cycle ,Up-Regulation ,030104 developmental biology ,Oncology ,Gene Knockdown Techniques ,030220 oncology & carcinogenesis ,embryonic structures ,Cancer research ,biology.protein ,Biomarkers - Abstract
Insulin-like growth factor-1 (IGF-1), a small polypeptide hormone similar to insulin in protein structures, has been identified as an activator of epithelial-mesenchymal transition (EMT) pathways in several types of cancers. As a member of the inhibitor of apoptosis protein (IAP) family, survivin is implicated in the EMT of some cancers. However, the role of survivin on IGF-1-mediated EMT of hepatocellular carcinoma (HCC) has not been clarified. In the present study, we demonstrated that survivin was involved in the EMT process induced by IGF-1 in HCC cell line SMMC7721. With administration of different concentrations of IGF-1, survivin mRNA and protein expression were significantly increased and stimulated EMT in the tested cell line, while the increased invasive and migratory abilities of HCC cells and activation of the EMT process induced by IGF-1 were reversed after silencing of survivin expression by transfecting small interfering RNA. This was further confirmed by the observation of morphological changes, the decrease of invasive and migratory abilities and the downregulation of EMT markers, N-cadherin, vimentin and Snail, and the upregulation of E-cadherin. In conclusion, survivin may play a vital role in the IGF-1 signaling pathway by mediating EMT in HCC through the upregulation of the expression of EMT markers, and the knockdown of survivin expression may suppress the metastasis of HCC, which may provide new insights for the molecular therapy of HCC patients in clinical treatment.
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- 2018
4. Low Expression of miR-448 Induces EMT and Promotes Invasion by Regulating ROCK2 in Hepatocellular Carcinoma
- Author
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Fangfeng Liu, Hongguang Li, Jun Lu, Hong Chang, Chaoqun Ma, Xu Zhou, and Huaqiang Zhu
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Oncology ,medicine.medical_specialty ,Carcinoma, Hepatocellular ,Epithelial-Mesenchymal Transition ,Physiology ,Cell ,Biology ,lcsh:Physiology ,lcsh:Biochemistry ,ROCK2 ,Invasion ,Western blot ,Cell Line, Tumor ,Internal medicine ,microRNA ,medicine ,Carcinoma ,Humans ,lcsh:QD415-436 ,Neoplasm Invasiveness ,Epithelial–mesenchymal transition ,HCC ,Regulation of gene expression ,rho-Associated Kinases ,Gene knockdown ,lcsh:QP1-981 ,medicine.diagnostic_test ,miR-448 ,Liver Neoplasms ,EMT ,medicine.disease ,digestive system diseases ,Gene Expression Regulation, Neoplastic ,MicroRNAs ,medicine.anatomical_structure ,Liver ,Hepatocellular carcinoma ,Cancer research - Abstract
Background/Aims: miR-448 has been reported to exhibit abnormal expression in hepatocellular carcinoma (HCC), however, the essential role of miR-448 in HCC progression is still unclear. Methods: real-time PCR was used to detect the expression of miRNAs and candidate genes in HCC samples (n=117). miR-448 mimics and inhibitor were tansfected in human HCC cells. The transwell assay was used to examine the cell invasive ability. The regulation mechanism was confirmed by luciferase reporter assay. The markers of EMT were detected by using Western blot. Results: miR-448 was decreased in HCC samples and associated with HCC development. Inhibition of miR-448 significantly promoted cell invasion, while the effect of miR-448 up-regulation was reverse. miR-448 could regulate ROCK2 in hepatocellular carcinoma. Knockdown of ROCK2 expression partially reversed the effect of miR-448 inhibitor. Abnormal expression of miR-448 could regulate the markers of epithelial-mesenchymal transition (EMT). Conclusions: miR-448 may contribute to the progression of HCC via regulating ROCK2 expression.
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- 2015
5. miR-1299 suppresses cell proliferation of hepatocellular carcinoma (HCC) by targeting CDK6
- Author
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Xie Song, Hengjun Gao, Hong Chang, Chaoqun Ma, Huaqiang Zhu, Guangchuan Wang, Xu Zhou, Hongguang Li, Fangfeng Liu, Jin-Ben Ma, and Jun Lu
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0301 basic medicine ,Carcinoma, Hepatocellular ,Down-Regulation ,03 medical and health sciences ,0302 clinical medicine ,Downregulation and upregulation ,Cell Line, Tumor ,microRNA ,Humans ,MTT assay ,Cell Proliferation ,Pharmacology ,Gene knockdown ,biology ,Base Sequence ,Cell growth ,Kinase ,Liver Neoplasms ,General Medicine ,Cyclin-Dependent Kinase 6 ,Cell cycle ,Cell biology ,Gene Expression Regulation, Neoplastic ,MicroRNAs ,030104 developmental biology ,030220 oncology & carcinogenesis ,Gene Knockdown Techniques ,biology.protein ,Cyclin-dependent kinase 6 - Abstract
microRNA (miRNA) plays critical role in HCC initiation and development, many miRNAs have been reported to regulate HCC progression. In this study, we studied the role of miR-1299 in cell proliferation of HCC. We found miR-1299 was significantly downregulated in HCC cells and tissues. miR-1299 overexpression inhibited cell proliferation and arrested cell cycle in G0/G1 phase analyzed by MTT assay, soft agar assay, BrdU cell proliferation assay and cell cycle assay, while miR-1299 knockdown promoted cell proliferation and accelerated G1/S transition. Further analysis suggested the key regulator of G1/S transition, cyclin-dependent kinase 6 (CDK6) was the target of miR-1299, miR-1299 inhibited CDK6 expression and bound to the 3'UTR of CDK6. When double knockdown of miR-1299 and CDK6 promoted cell proliferation copied the phenotype caused by miR-1299 overexpression, suggesting miR-1299 inhibits cell proliferation by targeting CDK6. In summary, our data revealed miR-1299 inhibits cell proliferation, and might be a target for HCC therapy.
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- 2016
6. Common Variants of the Prostaglandin-Endoperoxide Synthase 2 Gene and Hepatocellular Carcinoma Susceptibility
- Author
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Huaqiang Zhu, Hong Chang, Xu Zhou, Jin-Hua Hu, Jun Lu, Fangfeng Liu, and Hongguang Li
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Male ,medicine.medical_specialty ,Pathology ,Carcinoma, Hepatocellular ,Genotype ,Gastroenterology ,White People ,Prostaglandin-endoperoxide synthase 2 ,chemistry.chemical_compound ,Asian People ,Internal medicine ,Genetic variation ,medicine ,Humans ,Genetic Predisposition to Disease ,Gene ,ATP synthase ,biology ,business.industry ,Liver Neoplasms ,Case-control study ,Genetic Variation ,General Medicine ,medicine.disease ,digestive system diseases ,chemistry ,Cyclooxygenase 2 ,Hepatocellular carcinoma ,Case-Control Studies ,biology.protein ,Biomarker (medicine) ,Female ,business ,Systematic Review and Meta-Analysis ,Research Article - Abstract
Hepatocellular carcinoma (HCC) is a heterogeneous disease with substantial genetic constitution. Previous work has evaluated the effect of prostaglandin-endoperoxide synthase 2 (PTGS2) variants (−765G/C, −1195A/G, and +8473T/C) on the development of HCC, but the conclusions are inconsistent. We conducted a meta-analysis in this work. Data from 7 case–control studies were combined to assess the association between PTGS2 variants and HCC. The risk of HCC (OR and 95% CI) was estimated using either the fixed- or the random-effects model according to the Q test. No significant association was identified for −765G/C and +8473T/C. However, we identified a significantly decreased risk in relation to the GG genotype of −1195A/G (OR = 0.70, 95% CI = 0.50–0.98 for GG versus AA). We also observed a similar decrease (OR = 0.47, 95% CI = 0.23–0.95 for GG versus AA) in Caucasian samples. Variant −1195A/G in the promoter PTGS2 may protect against the malignant progression of HCC. This significant association suggests that −1195A/G could be used as a biomarker of HCC.
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- 2015
7. Aberrant Expression of CCAT1 Regulated by c-Myc Predicts the Prognosis of Hepatocellular Carcinoma
- Author
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Fangfeng Liu, Jun Lu, Hong Chang, Chaoqun Ma, Xu Zhou, Hongguang Li, and Huaqiang Zhu
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Cancer Research ,Chromatin Immunoprecipitation ,Carcinoma, Hepatocellular ,Epidemiology ,Colorectal cancer ,Blotting, Western ,Bioinformatics ,Real-Time Polymerase Chain Reaction ,Proto-Oncogene Proteins c-myc ,Carcinoma ,medicine ,Biomarkers, Tumor ,Humans ,Promoter Regions, Genetic ,Neoplasm Staging ,Regulation of gene expression ,business.industry ,Liver Neoplasms ,Public Health, Environmental and Occupational Health ,Cancer ,Hep G2 Cells ,medicine.disease ,Prognosis ,digestive system diseases ,Gene Expression Regulation, Neoplastic ,Survival Rate ,Real-time polymerase chain reaction ,Oncology ,Hepatocellular carcinoma ,Cancer research ,Disease Progression ,Biomarker (medicine) ,RNA, Long Noncoding ,Neoplasm Recurrence, Local ,business ,Chromatin immunoprecipitation - Abstract
Background CCAT1 has been reported to be linked with pathogenesis of malignancies including colon cancer and gastric cancer. However, the regulatory effect of CCAT1 in hepatocellular carcinoma (HCC) remains unclear. The purpose of this research was to identify any role of CCAT1 in the progression of HCC. Materials and methods Real time-PCR was performed to test the relative expression of CCAT1 in HCC tissues. A computation screen of CCAT1 promoter was conducted to search for transcription-factor-binding sites. The association of c-Myc with CCAT1 promoter in vivo was tested by Pearson correlation analysis and chromatin immunoprecipitation assay. Additionally, Kaplan-Meier analysis and Cox proportional hazards analyses were performed. Results c-Myc directly binds to the E-box element in the promoter region of CCAT, and when ectopically expressed increases promoter activity and expression of CCAT1. Moreover, Kaplan-Meier analysis demonstrated that the patients with low expression of CCAT1 demonstrated better overall and relapse-free survival compared with the high expression group. Cox proportional hazards analyses showed that CCAT1 expression was an independent prognostic factor for HCC patients. Conclusions The findings demonstrated CCAT1, acting as a potential biomarker in predicting the prognosis of HCC, is regulated by c-Myc.
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- 2015
8. Relevance between HLA-DP gene rs2281388 polymorphism and hepatocellular carcinoma risk
- Author
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Fangfeng, Liu, Jianlu, Wang, Hong, Chang, Jun, Lu, and Hongguang, Li
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Male ,HLA-DP Antigens ,Carcinoma, Hepatocellular ,Genotype ,Liver Neoplasms ,Middle Aged ,Polymerase Chain Reaction ,Polymorphism, Single Nucleotide ,Asian People ,Risk Factors ,Case-Control Studies ,Humans ,Female ,Genetic Predisposition to Disease ,Original Article ,Aged - Abstract
Purpose: We carried out this study to find out the relevance between rs2281388 T/C polymorphism of human leukocyte antigen (HLA) gene and hepatocellular carcinoma (HCC) risk in Chinese Han population. Methods: The method of polymerase chain reaction (PCR) was applied to amplify the genomic DNA. Then the PCR products were sequenced to test the HLA-DP gene rs2281388T/C polymorphism of the case and control groups. Odds ratios (ORs) and 95% confidence interval (95% CIs) were utilized to evaluate the potential correlation between rs2281388 variants and HCC risk. Results: We analyzed the rs2281388 polymorphism distribution among the clinical pathological features. The results showed that there existed a significant statistic correlation between rs2281388T/C polymorphism of HLA-DP gene and HBsAg feature, and no significant correlation was found between rs2281388 and other clinical features. Further analysis showed that the TT genotype of rs2281388 was significantly correlated with HCC risk, and the same to T allele, but there was no significant difference of CT genotype distribution in case and control groups. Conclusion: TT genotype and T allele of HLA-DP gene rs2281388 polymorphism may increase the risk of HCC.
- Published
- 2015
9. Two polymorphisms of USF1 gene (-202GA and -844CT) may be associated with hepatocellular carcinoma susceptibility based on a case-control study in Chinese Han population
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Hongguang Li, Xu Zhou, Hong Chang, Chaoqun Ma, Jun Lu, Huaqiang Zhu, and Fangfeng Liu
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Adult ,Male ,Cancer Research ,Carcinoma, Hepatocellular ,Single-nucleotide polymorphism ,Biology ,Polymorphism, Single Nucleotide ,Asian People ,Genotype ,medicine ,Humans ,Genetic Predisposition to Disease ,Allele ,Genetic Association Studies ,Genetics ,Liver Neoplasms ,Case-control study ,Hematology ,General Medicine ,Odds ratio ,Middle Aged ,medicine.disease ,Molecular biology ,Genotype frequency ,Oncology ,Hepatocellular carcinoma ,Case-Control Studies ,Population Surveillance ,Upstream Stimulatory Factors ,Female ,Liver cancer - Abstract
Hepatocellular carcinoma (HCC) is a prototype of liver cancer, which is closely related to manifested metabolism of lip and glucose. Upstream transcription factor 1 (USF1) is an important transcription factor in human genome, and it regulates the expression of multiple genes associated with lipid and glucose metabolism. This study aims at investigating the correlation between seven common USF1 polymorphisms (i.e., -1994 G>A, -202 G>A, 7998 A>G, -844 C>T, 9042 C>G, 9441 T>C, and -2083 G>A) and the risk of HCC. Elucidation of the interaction might be of vital importance to the diagnosis and prognosis of HCC. One hundred and fifty-five HCC patients and 160 healthy controls from a Chinese Han population were involved in this study. Tag single-nucleotide polymorphisms (SNPs) were identified with reference to CBI-dbSNP and HapMap databases. DNA was extracted from blood samples, and matrix-assisted laser desorption-ionization time-of-flight mass spectrometry (MALDI-TOF-MS) was conducted to determine the polymorphisms of USF1. Odds ratio (OR) and 95% confidence interval were applied to evaluate the difference of genotype distribution. Seven SNPs were selected to be representatives. No significant difference was observed concerning -1994 G>A, 7998 A>G, 9042 C>G, 9441 T>C, and -2083 G>A polymorphisms (all P > 0.05). A significantly elevated genotype frequency regarding -202 G>A polymorphism was observed in HCC patients [AA vs. GG: OR 2.13 (1.13-4.01), P = 0.019; AA vs. GG+GA: OR 2.22 (1.32-3.75), P = 0.003; A allele vs. G allele: OR 1.46 (1.07-2.01), P = 0.018]. Subjects carrying mutant -844 C>T genotypes also had a higher risk of HCC [CT vs. CC: OR 1.88 (1.17-3.04), P = 0.009; CT+TT vs. CC: OR 1.83 (1.17-2.86), P = 0.008; T allele vs. C allele: OR 1.49 (1.06-2.09), P = 0.020]. Further studies are recommended to validate our findings in different ethnicity and to clarify the functional relationship between USF1 polymorphisms and the susceptibility of HCC.
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- 2014
10. Identification of hepatocellular carcinoma-associated hub genes and pathways by integrated microarray analysis
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Hong Chang, Jianlu Wang, Jun Lu, Fangfeng Liu, and Hongguang Li
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Cancer Research ,Carcinoma, Hepatocellular ,Gene regulatory network ,Down-Regulation ,Biology ,Bioinformatics ,Malignancy ,Real-Time Polymerase Chain Reaction ,Japan ,Carcinoma ,medicine ,Humans ,Gene Regulatory Networks ,Protein Interaction Maps ,Regulation of gene expression ,Microarray analysis techniques ,Reverse Transcriptase Polymerase Chain Reaction ,Gene Expression Profiling ,Liver Neoplasms ,Computational Biology ,General Medicine ,Oncogenes ,medicine.disease ,Microarray Analysis ,Up-Regulation ,Gene Expression Regulation, Neoplastic ,Real-time polymerase chain reaction ,Oncology ,Hepatocellular carcinoma ,Cancer research ,Identification (biology) ,Signal Transduction - Abstract
Aims and Background Hepatocellular carcinoma (HCC) is a dismal malignancy associated with multiple molecular changes. The purpose of this study was to identify the differentially expressed genes and analyze the biological processes related to HCC. Methods and Study Design Datasets of HCC were obtained from the NCBI Gene Expression Omnibus. Integrated analysis of differentially expressed genes was performed using the INMEX program. Then Gene Ontology enrichment analyses and pathway analysis were performed based on the Gene Ontology website and Kyoto Encyclopedia of Genes and Genomes. A protein-protein interaction network was constructed using the Cytoscape software; the netwerk served to find hub genes for HCC. Real-time RT-PCR was used to validate the microarray data for hub genes. Results We identified 273 genes that were differentially expressed in HCC. Gene Ontology enrichment analyses revealed response to cadmium ion, cellular response to cadmium ion, and cellular response to zinc ion for these genes. Pathway analysis showed that significant pathways included fatty acid metabolism, butanoate metabolism, and PPAR signaling pathway. The protein-protein interaction network indicated that CDH1, ECHS1, ACAA1, MT2A, and MYC were important genes which participated in many interactions. Experimental validation of the role of four upregulated genes ( ECHS1, ACAA1, MT2A and MYC) in the progression of HCC was carried out. Conclusions Our study displayed genes that were consistently differentially expressed in HCC. The biological pathways and protein-protein interaction networks associated with those genes were also identified. We predicted that CDH1, ECHS1, ACAA1, MT2A, and MYC might be target genes for diagnosing HCC.
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- 2014
11. Significant Association Between Adiponutrin and Hepatocellular Carcinoma Risk
- Author
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Hong Chang, Huaqiang Zhu, Xu Zhou, Hongguang Li, Jin-Hua Hu, Fangfeng Liu, and Jun Lu
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Pathology ,medicine.medical_specialty ,Alcoholic liver disease ,Carcinoma, Hepatocellular ,Subgroup analysis ,Gastroenterology ,Internal medicine ,Nonalcoholic fatty liver disease ,Humans ,Medicine ,Genetic Predisposition to Disease ,Adiponutrin ,education ,education.field_of_study ,Polymorphism, Genetic ,business.industry ,Liver Neoplasms ,Membrane Proteins ,Lipase ,General Medicine ,Publication bias ,Odds ratio ,medicine.disease ,Confidence interval ,Hepatocellular carcinoma ,business ,Systematic Review and Meta-Analysis ,Research Article - Abstract
ADPN I148M polymorphism has been consistently reported to play a role in liver-associated diseases, such as alcoholic liver disease, chronic hepatitis C, and liver fat and fibrosis in nonalcoholic fatty liver disease. This significant association was also indicated in a series of hepatocellular carcinoma (HCC) studies, where the significance may be affected due to the small sample sizes. The aim of this study was to reexamine the ADPN-HCC association by use of meta-analysis. Biweekly computer-based literature searches plus manual screening were undertaken in an effort to identify all studies that met the predefined inclusion criteria. The Mantel–Haenszel method was selected to estimate risk effects (odds ratio [OR] and 95% confidence interval [CI]). To examine reliability of the pooled risk effects, we additionally performed sensitivity analysis and publication bias tests. Ten studies (1335 HCC patients and 2927 HCC-free controls) were identified for the meta-analysis. We found significantly increased risk of HCC attributable to presence of ADPN I148M polymorphism, with the highest risk associated with the M/M genotype under the recessive model of inheritance (OR = 2.23, 95% CI = 1.87–2.67, between-study heterogeneity: P = 0.468). The significant increase persisted in Caucasian and African when data were stratified by ethnicity. Subgroup analysis according to source of controls revealed similar risk effects. Our meta-analysis indicates that I148M polymorphism in the ADPN gene may independently contribute to the progression of HCC irrespective of the etiologies.
- Published
- 2015
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