15 results on '"Cui‐Ling Ding"'
Search Results
2. Chikungunya virus and autoimmunity: Consensus immune epitope analysis between chikungunya virus and arthritis
- Author
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Gen Miao, Yangang Liu, Zhong-Tian Qi, Cui-Ling Ding, and Wen Wang
- Subjects
Consensus ,business.industry ,Arthritis ,Immunology ,Autoimmunity ,medicine.disease_cause ,medicine.disease ,Virology ,Epitope ,Virus ,Epitopes ,Immune system ,medicine ,Immunology and Allergy ,Humans ,Chikungunya ,business ,Chikungunya virus - Published
- 2020
3. Retinoic acid induced 16 deficiency exacerbates high-fat diet-induced steatohepatitis in mice
- Author
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Zhong-Tian Qi, Wen Wang, Chun-Lin Qian, Hailin Tang, and Cui-Ling Ding
- Subjects
0301 basic medicine ,Male ,medicine.medical_specialty ,Cirrhosis ,Clinical Biochemistry ,Retinoic acid ,Inflammation ,Apoptosis ,Diet, High-Fat ,Biochemistry ,03 medical and health sciences ,chemistry.chemical_compound ,Mice ,0302 clinical medicine ,Lipocalin-2 ,Non-alcoholic Fatty Liver Disease ,Internal medicine ,medicine ,Animals ,Fatty acid synthesis ,Chemokine CCL2 ,Liver injury ,Mice, Knockout ,business.industry ,Macrophages ,digestive, oral, and skin physiology ,Fatty liver ,Fatty Acids ,food and beverages ,nutritional and metabolic diseases ,Proteins ,Cell Biology ,General Medicine ,medicine.disease ,Lipid Metabolism ,Mice, Inbred C57BL ,030104 developmental biology ,Endocrinology ,chemistry ,Gene Expression Regulation ,030220 oncology & carcinogenesis ,lipids (amino acids, peptides, and proteins) ,medicine.symptom ,Steatohepatitis ,business - Abstract
Non-alcoholic fatty liver disease (NAFLD) associated with obesity may progress to non-alcoholic steatohepatitis, cirrhosis and hepatocellular carcinoma (HCC). Retinoic acid induced 16 (RAI16) plays an important role in cell apoptosis and is also a potential marker for HCC. Here we aimed to test the effect of RAI16 deficiency on liver pathology in high-fat diet (HFD) fed mice. Wild type (WT) and RAI16 knockout (RAI16-/-) C57BL/6 mice were fed with HFD or chow for up to 12 months. With consumption of HFD diet, RAI16-/- mice on HFD developed much more excess fatty liver within 4 months than WT mice on HFD. The expressions of fatty acid synthesis associated molecules Ppar-γ, Srebp-1c and Fas were further increased in RAI16-/- mice compared with WT mice on HFD. Macrophage infiltration related molecules Mcp-1 and F4/80 and pro-inflammatory factor Lcn2 were significantly increased in RAI16-/- mice compared with WT mice on HFD. Conclusively, RAI16 deficiency exacerbated HFD-induced liver injury, associated with increased inflammation. These findings indicate that RAI16 plays an important role in HFD-induced liver pathology and might be considered as a target for treatment of NAFLD. SIGNIFICANCE: 1. RAI16-/- mice on HFD developed much more excess fatty liver. 2. RAI16-/- mice showed more macrophage infiltration and proinflammation.
- Published
- 2020
4. Identification of retinoid acid induced 16 as a novel androgen receptor target in prostate cancer cells
- Author
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Wen Wang, Zhong-Tian Qi, Cui-Ling Ding, and Chun-Lin Qian
- Subjects
0301 basic medicine ,Male ,030209 endocrinology & metabolism ,Adenocarcinoma ,medicine.disease_cause ,Biochemistry ,03 medical and health sciences ,Prostate cancer ,0302 clinical medicine ,Endocrinology ,DU145 ,Cell Line, Tumor ,LNCaP ,medicine ,Humans ,Viability assay ,Promoter Regions, Genetic ,Molecular Biology ,Gene knockdown ,Oncogene ,Chemistry ,Prostatic Neoplasms ,Proteins ,Metribolone ,medicine.disease ,Androgen receptor ,Gene Expression Regulation, Neoplastic ,030104 developmental biology ,Receptors, Androgen ,PC-3 Cells ,Cancer research ,Androgens ,Carcinogenesis ,Protein Binding - Abstract
Background Retinoid acid induced 16 (RAI16) was reported to enhance tumorigenesis in hepatocellular carcinoma (HCC). The androgen receptor (AR) is a nuclear hormone receptor that functions as a critical oncogene in several cancer progressions. However, whether RAI16 is a candidate AR target gene that may involve in prostate cancer progression was unclear. Materials & methods RAI16 expression was detected in prostate cancer cells with or without the AR agonist R1881 treatment by quantitative RT-PCR and Western blot. Direct AR binding to the RAI16 promoter was tested using AR chromatin immunoprecipitation (ChIP) and luciferase assay. Cell viability and colony formation assays in response to R1881 were analyzed in cells with RAI16 knockdown by specific siRNA. Results The expression of RAI16 was high in LNCaP(AI), LNCaP(AD), C4-2 expressing AR, but low in Du145 and Pc-3 cells without AR expressing. In addition, the expression of RAI16 could be induced by 10 nM R1881 treatment LNCaP(AD) and C4-2 cells, but inhibited by AR specific siRNA treatment. Furthermore, AR binds directly to ARE3 (−2003~-1982bp) of RAI16 promoter region by ChIP and luciferase assay. RAI16 knockdown inhibited the enhancement of cell viability and colony formation of AR stimulation. Conclusions We demonstrate for the first time that RAI16 is a direct target gene of AR. RAI16 may involved in cell growth of prostate cancer cells in response to AR signaling.
- Published
- 2019
5. Retinoid acid induced 16 deficiency aggravates colitis and colitis-associated tumorigenesis in mice
- Author
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Zhong-Tian Qi, Wen Wang, Yu-Lin Xu, Chun-Lin Qian, and Cui-Ling Ding
- Subjects
Cancer Research ,Carcinoma, Hepatocellular ,medicine.drug_class ,Colorectal cancer ,Carcinogenesis ,Colon ,Immunology ,Inflammation ,medicine.disease_cause ,Inflammatory bowel disease ,Article ,Cellular and Molecular Neuroscience ,chemistry.chemical_compound ,Mice ,medicine ,Animals ,Humans ,Retinoid ,lcsh:QH573-671 ,Colitis ,Intestinal Mucosa ,Barrier function ,lcsh:Cytology ,Chemistry ,Azoxymethane ,Dextran Sulfate ,Liver Neoplasms ,Proteins ,Cell Biology ,Chronic inflammation ,medicine.disease ,Inflammatory Bowel Diseases ,digestive system diseases ,Neoplasm Proteins ,Gene Expression Regulation, Neoplastic ,Disease Models, Animal ,Cell Transformation, Neoplastic ,Cancer research ,medicine.symptom ,Colorectal Neoplasms ,Signal Transduction - Abstract
Inflammatory bowel disease (IBD) and colitis-associated colorectal cancer (CAC) is a serious health issue, but etiopathological factors remain unclear. Although some studies reported the roles of Retinoid acid induced 16 (RAI16) in the tumorigenesis of hepatocellular carcinoma and PKA signaling, the roles of RAI16 in IBD and CRC are undressed. RAI16−/− mice were generated and the roles of RAI16 were addressed in dextran sodium sulfate (DSS) or azoxymethane (AOM)-DSS induced IBD or CAC mouse models, respectively. At first, RAI16−/− mice were viable, fertile with no apparent defects. Then, it was found that RAI16−/− mice were more susceptibility to colitis induced by DSS than wild type (WT) littermates, which was evaluated by disease activity index and histological score. Furthermore, the expressions of tissues repair associated molecules Cox2, Ereg and MMP-10 were significantly decreased in RAI16−/− colon under DSS treatment. Gut barrier related genes including antimicrobial peptides Reg3b and Reg3g and intestinal mucus genes Muc4, Muc6 and Muc20 were reduced in RAI16−/− colon. These findings indicated that RAI16 may function to affect genes involved in intestinal barrier function and immunoprotective inflammation. Accordingly, RAI16−/− mice displayed significantly increased tumor burden compared with WT mice assessed in CAC model induced by AOM/DSS. Much more Ki67 + nuclei were observed in RAI16−/− tumors suggesting RAI16 to be critical in colonic cell proliferation during tumorigenesis. Conclusively, we demonstrate the roles of RAI16 in colonic inflammation and inflammation-associated tumorigenesis by using a novel RAI16−/− mouse model for the first time.
- Published
- 2019
6. HCV infection induces the upregulation of miR-221 in NF-κB dependent manner
- Author
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Cui-Ling Ding, Gang Xu, Lan-Juan Zhao, Ping Zhao, Wen Wang, Hao Ren, and Zhong-Tian Qi
- Subjects
Adult ,Male ,Cancer Research ,Dependent manner ,Aspartate transaminase ,Hepacivirus ,Biology ,Positive correlation ,Cell Line ,Young Adult ,chemistry.chemical_compound ,Downregulation and upregulation ,Pyrrolidine dithiocarbamate ,Virology ,medicine ,Humans ,Aged ,NF-kappa B ,Cancer ,NF-κB ,Middle Aged ,medicine.disease ,Hepatitis C ,digestive system diseases ,Up-Regulation ,MicroRNAs ,Infectious Diseases ,Gene Expression Regulation ,chemistry ,Biological significance ,Host-Pathogen Interactions ,Immunology ,biology.protein ,Female - Abstract
The upregulation of miR-221 has been reported in variety of cancer, including HCV associated HCC, the mechanism of upregulation of miR-221 however remains unclear. In this study, it was found that miR-221 was significantly upregulated in serum of patients with HCV associated chronic hepatitis (cHCV), which suggested the possible biological significance of miR-221 in HCV infection. Important, the upregulated miR-221 was positive correlation with serum miR-122, alanine aminotransferase (ALT) and aspartate transaminase (AST), which are reported as biomarkers for liver injuries. Further studies indicated that HCVcc infection activated nuclear factor-kappa B (NF-κB) and the upregulation of miR-221 by HCVcc infection could totally blocked by NF-κB inhibitor (pyrrolidine dithiocarbamate, PDTC). In conclusion, HCVcc infection could upregulate the expression of miR-221 in NF-κB dependent manner.
- Published
- 2015
7. Comparison of Formulas Based on Lipid Emulsions of Olive Oil, Soybean Oil, or Several Oils for Parenteral Nutrition: A Systematic Review and Meta-Analysis
- Author
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Sen-Hai Xue, Li-Juan Sun, Wen Wang, Li-Li Sun, Meng-Ying Li, Yu-Jie Dai, Cui-Ling Ding, Chang-Hai Zhao, Yu-Cheng Su, and Feng Yan
- Subjects
0301 basic medicine ,Fat Emulsions, Intravenous ,Parenteral Nutrition ,food.ingredient ,Medicine (miscellaneous) ,Aspartate transaminase ,Reviews ,Soybean oil ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,food ,Fish Oils ,otorhinolaryngologic diseases ,Humans ,Food science ,Olive Oil ,Randomized Controlled Trials as Topic ,chemistry.chemical_classification ,030109 nutrition & dietetics ,Nutrition and Dietetics ,Evidence-Based Medicine ,biology ,Fatty Acids, Essential ,business.industry ,Fish oil ,Biotechnology ,Soybean Oil ,Oleic acid ,chemistry ,Alanine transaminase ,Docosahexaenoic acid ,biology.protein ,030211 gastroenterology & hepatology ,Liver function ,business ,Deficiency Diseases ,Food Science ,Polyunsaturated fatty acid - Abstract
Many studies have reported that olive oil-based lipid emulsion (LE) formulas of soybean oil, medium-chain triglycerides, olive oil, and fish oil (SMOF) may be a viable alternative for parenteral nutrition. However, some randomized controlled clinical trials (RCTs) have raised concerns regarding the nutritional benefits and safety of SMOFs. We searched principally the MEDLINE, Cumulative Index to Nursing and Allied Health Literature, Scopus, EMBASE, and Cochrane Central Register of Controlled Trials databases from inception to March 2014 for the relevant literature and conducted a meta-analysis of 15 selected RCTs that 1) compared either olive oil- or SMOF-based LEs with soybean oil-based LEs and 2) reported plasma concentrations of α-tocopherol, oleic acid, and ω-6 (n-6) and ω-3 (n-3) long-chain polyunsaturated fatty acids (PUFAs) and liver concentrations of total bilirubin and the enzymes alanine transaminase, aspartate transaminase, alkaline phosphatase, and γ-glutamyl transferase. The meta-analysis suggested that SMOF-based LEs were associated with higher plasma concentrations of plasma α-tocopherol, oleic acid, and the ω-3 PUFAs eicosapentaenoic and docosahexaenoic acid. Olive oil- and SMOF-based LEs correlated with lower plasma concentrations of long-chain ω-6 PUFAs and were similar to soybean oil-based LEs with regard to their effects on liver function indicators. In summary, olive oil- and SMOF-based LEs have nutritional advantages over soybean oil-based LEs and are similarly safe. However, their performance in clinical settings requires further investigation.
- Published
- 2017
8. MiR-221 accentuates IFN׳s anti-HCV effect by downregulating SOCS1 and SOCS3
- Author
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Hao Ren, Jing Wang, Fang Yang, Wen Wang, Gang Xu, Cui-Ling Ding, and Ping Zhao
- Subjects
Adult ,Male ,Hepatitis C virus ,medicine.medical_treatment ,Down-Regulation ,Suppressor of Cytokine Signaling Proteins ,Hepacivirus ,Biology ,medicine.disease_cause ,Cell Line ,Suppressor of Cytokine Signaling 1 Protein ,Virology ,medicine ,SOCS1 ,Humans ,SOCS3 ,NS5A ,IFN-α ,Aged ,Suppressor of cytokine signaling 1 ,JAK-STAT signaling pathway ,Interferon-alpha ,Mir-221 ,Hepatitis C, Chronic ,Middle Aged ,medicine.disease ,digestive system diseases ,MicroRNAs ,Cytokine ,Suppressor of Cytokine Signaling 3 Protein ,Hepatocellular carcinoma ,HCV ,Cancer research ,Female ,Carcinogenesis - Abstract
MiR-221 was reported to be upregulated and play roles in tumorigenesis of hepatitis C virus (HCV) associated hepatocellular carcinoma (HCC). However, the role of miR-221 in HCV infection remains unknown. In this study, it was found that miR-221 was upregulated in serum of HCV chronic hepatitis patients and Huh7.5.1 cells infected with HCVcc. Further studies indicated that miR-221 mimic could accentuate anti-HCV effect of IFN-α in HCVcc model, miR-221 mimic could further repressed 10% HCV RNA expression and 35–42% HCV core or NS5A protein expression in HCVcc infected Huh7.5.1 cells treated with 100 IU/mL IFN-α, and miR-221 inhibitor resulted in the reverse effects. Furthermore, two members of suppressor of cytokine signaling (SOCS) family, SOCS1 and SOCS3, which are well established inhibitory factors on IFN/JAK/STAT pathway, were identified as the targets of miR-221 and were involved in the effect of miR-221. In conclusion, miR-221 could accentuate IFN׳s anti-HCV effect by targeting SOCS1 and SOCS3.
- Published
- 2014
- Full Text
- View/download PDF
9. Anchoring of both PKA-RIIα and 14-3-3θ regulates retinoic acid induced 16 mediated phosphorylation of heat shock protein 70
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Shi-Ying Zhu, Cui-Ling Ding, Wen Wang, Ping Zhao, Zhong-Tian Qi, Gang Xu, Hailin Tang, Lan-Juan Zhao, and Hao Ren
- Subjects
PKA-RIIα ,Carcinoma, Hepatocellular ,Immunoprecipitation ,Cell Survival ,Protein subunit ,Retinoic acid ,A Kinase Anchor Proteins ,Apoptosis ,Biology ,Cell Line ,Serine ,chemistry.chemical_compound ,AKAP ,Tandem Mass Spectrometry ,Cyclic AMP-Dependent Protein Kinase RIIalpha Subunit ,Humans ,HSP70 Heat-Shock Proteins ,Phosphorylation ,Kinase ,Liver Neoplasms ,RAI16 ,Proteins ,Molecular biology ,14-3-3θ ,Cell Transformation, Neoplastic ,HEK293 Cells ,Oncology ,chemistry ,14-3-3 Proteins ,Fam160B2 ,Signal transduction ,Signal Transduction ,Research Paper - Abstract
// Cui-Ling Ding 1,* , Gang Xu 1,* , Hai-Lin Tang 1 , Shi-Ying Zhu 1 , Lan-Juan Zhao 1 , Hao Ren 1 , Ping Zhao 1 , Zhong-Tian Qi 1 and Wen Wang 1 1 Department of Microbiology, Shanghai Key Laboratory of Medical Biodefense, Second Military Medical University, Shanghai, China * These authors have contributed equally to this work Correspondence to: Zhong-Tian Qi, email: // Wen Wang, email: // Keywords : RAI16, Fam160B2, AKAP, PKA-RIIα, 14-3-3θ Received : January 19, 2015 Accepted : March 05, 2015 Published : March 30, 2015 Abstract Our previous study reported that retinoic acid induced 16 (RAI16) could enhance tumorigenesis in hepatocellular carcinoma (HCC). However, the cellular functions of RAI16 are still unclear. In this study, by immunoprecipitation and tandem (MS/MS) mass spectrometry analysis, we identified that RAI16 interacted with the type II regulatory subunit of PKA (PKA-RIIα), acting as a novel protein kinase A anchoring protein (AKAP). In addition, RAI16 also interacted with heat shock protein 70 (HSP70) and 14-3-3θ. Further studies indicated that RAI16 mediated PKA phosphorylation of HSP70 at serine 486, resulting in anti-apoptosis events. RAI16 was also phosphorylated by the anchored PKA at serine 325, which promoted the recruitment of 14-3-3θ, which, in turn, inhibited RAI16 mediated PKA phosphorylation of HSP70. These findings offer mechanism insight into RAI16 mediated anti-apoptosis signaling in HCC.
- Published
- 2015
10. Small nucleolar RNA 113–1 suppresses tumorigenesis in hepatocellular carcinoma
- Author
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Cui-Ling Ding, Fang Yang, Hao Ren, Zhong-Tian Qi, Lan-Juan Zhao, Gang Xu, Wen Wang, and Ping Zhao
- Subjects
Adult ,Male ,Cancer Research ,Pathology ,medicine.medical_specialty ,Carcinoma, Hepatocellular ,MAP Kinase Signaling System ,Mice, Nude ,Biology ,medicine.disease_cause ,Mice ,Nude mouse ,Downregulation and upregulation ,Cell Line, Tumor ,medicine ,Animals ,Humans ,RNA, Small Nucleolar ,Phosphorylation ,Small nucleolar RNA ,Regulation of gene expression ,Research ,Liver Neoplasms ,RNA ,Hep G2 Cells ,DNA Methylation ,Middle Aged ,biology.organism_classification ,digestive system diseases ,Gene Expression Regulation, Neoplastic ,HEK293 Cells ,Oncology ,DNA methylation ,Cancer cell ,Cancer research ,Molecular Medicine ,Female ,Carcinogenesis ,Neoplasm Transplantation - Abstract
Background Emerging evidence suggests that small nucleolar RNAs (snoRNAs) are involved in tumorigenesis. The roles of small nucleolar RNA 113–1 (SNORD113-1) on the development of hepatocellular carcinoma (HCC) remain unknown. Methods The expression of SNORD113-1 was measured in 112 HCC tumor tissues using quantitative RT-PCR and compared with expression levels from with paired non-tumor tissues. The effects of SNORD113-1 on HCC tumorigenesis were investigated in HepG2 and Huh7 cells as well as a xenograft nude mouse model. CpG methylation within the promoter region of the SNORD113-1 gene was identified using Sodium bisulfite sequencing. Cancer pathway reporter investigate the mechanism by which SNORD113-1 suppressed tumorigenesis. Results SNORD113-1 expression was significantly downregulated in HCC tumors compared with adjacent non-tumor tissues, and downregulation of SNORD113-1 in HCC tumors was significantly associated with worse survival of patients. In addition, CpG methylation at the promoter region of the SNORD113-1 gene was higher in HCC tumors than adjacent non-tumor tissues. Functionally, SNORD113-1 suppressed cancer cell growth in HepG2 and Huh7 cells and in a xenograft nude mouse model. Furthermore, SNORD113-1 inactivated the phosphorylation of ERK1/2 and SMAD2/3 in MAPK/ERK and TGF-β pathways. Conclusions SNORD113-1 functions as a tumor suppressor role in HCC and may be important as a potential diagnostic and therapeutic target for HCC. Electronic supplementary material The online version of this article (doi:10.1186/1476-4598-13-216) contains supplementary material, which is available to authorized users.
- Published
- 2014
11. [Clinical significance of skin prick test for inhalant allergens in 3085 children with allergic diseases]
- Author
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Sheng-Quan, Cheng, Huan, Qiang, Cui-Ling, Ding, Kai-Li, Pan, Yu-Hong, Cao, Rong, Fu, and Ya-Nan, Ding
- Subjects
Male ,Adolescent ,Child, Preschool ,Hypersensitivity ,Humans ,Infant ,Female ,Allergens ,Child ,Skin Tests - Abstract
To investigate the main inhalant allergens and their distribution patterns in children with allergic diseases from Xi'an and the surrounding area and to provide evidence for the prevention and treatment of allergic diseases in children.Skin prick test was performed using liquid with 13 standardized allergens (ALK-ABELL, Denmark) on 3085 children from Xi'an and the surrounding area who were treated for allergic diseases between July 2006 and July 2011, to detect inhalant allergens.Of the 3085 patients, 1368 (44.34%) had positive SPT results, with the most prevalent inhalant allergen being Dermatophagoides pteronyssinus (804 cases, 26.06%), followed by Dermatophagoides farinae (793 cases, 25.71%), Blomia tropicalis (440 cases, 14.26%), mugwort (282 cases, 9.14%), and cat hair (204 cases, 6.61%). The positive rates were 28.66% in the4 years group, 41.85% in the 4-6 years group, and 58.61% in the 7-15 years group (P0.01). Males had a significantly higher SPT positive rate than females (47.78% vs 38.50%;P0.05). The SPT positive rate was highest in children with allergic rhinitis (72.41%), followed by bronchial asthma (62-25%), allergic dermatosis (45.83%), and allergic purpura (36.28%).In children from Xi'an and the surrounding area, the main inhalant allergens for allergic diseases include Dermatophagoides pteronyssinus, Dermatophagoides farinae, Blomia tropicalis, mugwort and cat hair. The SPT positive rate increases with age. Male children have a higher SPT positive rate than female children. The SPT positive rate is highest in children with allergic rhinitis.
- Published
- 2012
12. All-trans retinoic acid protects hepatocellular carcinoma cells against serum-starvation-induced cell death by upregulating collagen 8A2
- Author
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Wen Wang, Zhong-Tian Qi, Lan-Juan Zhao, Cui-Ling Ding, Ping Zhao, Gang Xu, and Hao Ren
- Subjects
Programmed cell death ,Carcinoma, Hepatocellular ,Blotting, Western ,Retinoic acid ,Apoptosis ,Tretinoin ,Biology ,Collagen Type VIII ,Real-Time Polymerase Chain Reaction ,Biochemistry ,Culture Media, Serum-Free ,chemistry.chemical_compound ,CYP26A1 ,Downregulation and upregulation ,Cell Movement ,Biomarkers, Tumor ,Cell Adhesion ,Tumor Cells, Cultured ,Humans ,RNA, Messenger ,Cell adhesion ,neoplasms ,Molecular Biology ,Oligonucleotide Array Sequence Analysis ,Reverse Transcriptase Polymerase Chain Reaction ,Gene Expression Profiling ,Cell Cycle ,Liver Neoplasms ,Cell migration ,Cell Biology ,Cell cycle ,Molecular biology ,Up-Regulation ,chemistry ,Starvation ,Cancer research - Abstract
As a therapeutic or chemopreventative agent for various cancers, all-trans retinoic acid (atRA) has been reported to inhibit growth, induce apoptosis or cause differentiation. It was found that atRA could protect hepatocellular carcinoma (HCC) cells against cell death induced by serum starvation. Furthermore, it was found that atRA could enhance cell adhesion, but had no effect on the cell cycle and apoptosis. Using an Illumina Human HT-12 v4 expression microarray, 207 upregulated and 173 downregulated genes were identified in HepG2 cells treated with atRA. The most upregulated genes are cytochrome P450 family 26 subfamily A polypeptide 1 (CYP26A1), histidine triad nucleotide binding protein 3 (HINT3), miR-1282 and cytochrome P450 family 26 subfamily B polypeptide 1 (CYP26B1), which showed more than fivefold greater expression. Using Gene Ontology analysis, the greatest significance was found in extracellular-matrix-related molecular functions and the cellular component in upregulated genes. The upregulation of collagen 8A2 (COL8A2) was further confirmed using quantitative RT-PCR and western blotting. Knockdown of COL8A2 blocked enhancement in the early stage of cell adhesion by atRA treatment. Re-expression of COL8A2 in COL8A2-knocked-down HCC cells reversed the effect of small interfering RNA-COL8A2. In addition, COL8A2 could increase HCC cell migration and invasion. Thus, COL8A2 was identified as the key protein involved in the enhancement of cell adhesion of atRA under serum-free conditions. In conclusion, atRA protects HCC cells against serum-starvation-induced cell death by enhancing cell adhesion, and COL8A2 plays an important role in HCC cell migration and invasion.
- Published
- 2012
13. [Cantharidin regulates intracellular ATP in G1/S-phase renal tubule epithelial cells]
- Author
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Qing, Shen, Yu-jia, Yao, Ru-ying, Li, Cui-ling, Ding, Li-chao, Hou, and Xu-de, Sun
- Subjects
Adenosine Triphosphate ,Kidney Tubules ,Animals, Newborn ,Swine ,Cantharidin ,G1 Phase ,Animals ,Epithelial Cells ,Enzyme Inhibitors ,Cell Hypoxia ,Cells, Cultured ,S Phase - Abstract
To study the mechanism of cantharidin in protecting F-actin microfilaments from disruption by hypoxic damage by observing the effects of cantharidin on intracellular ATP metabolism in G(1)/S-phase renal tubule epithelial cells (RTECs).G1-phase RTECs were divided into cantharidin-treated group, exposed to sodium cyanide (CN) and cantharidin, hypoxic-group with CN exposure and non-treated control group. ATP levels were measured in the 3 groups with high-performance liquid chromatography.The concentration of CN exposure for 1 h, ATP level in the RTECs with cantharidin treatment were significantly higher than that in both hypoxic and non-treated control groups (14.50+/-0.26 mmol/g protein, 4.25+/-0.11 mmol/g protein, 8.58+/-0.13 mmol/g protein, respectively, P0.01).Cantharidin prevents the disruption of the actin cytoskeleton in hypoxic damage by preventing abnormal intracellular ATP metabolism.
- Published
- 2004
14. Small nucleolar RNA 113-1 suppresses tumorigenesis in hepatocellular carcinoma.
- Author
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Gang Xu, Fang Yang, Cui-Ling Ding, Lan-Juan Zhao, Hao Ren, Ping Zhao, Wen Wang, and Zhong-Tian Qi
- Subjects
LIVER cancer ,NEOPLASTIC cell transformation ,XENOGRAFTS ,CANCER cell growth ,LABORATORY mice - Abstract
Background: Emerging evidence suggests that small nucleolar RNAs (snoRNAs) are involved in tumorigenesis. The roles of small nucleolar RNA 113-1 (SNORD113-1) on the development of hepatocellular carcinoma (HCC) remain unknown. Methods: The expression of SNORD113-1 was measured in 112 HCC tumor tissues using quantitative RT-PCR and compared with expression levels from with paired non-tumor tissues. The effects of SNORD113-1 on HCC tumorigenesis were investigated in HepG2 and Huh7 cells as well as a xenograft nude mouse model. CpG methylation within the promoter region of the SNORD113-1 gene was identified using Sodium bisulfite sequencing. Cancer pathway reporter investigate the mechanism by which SNORD113-1 suppressed tumorigenesis. Results: SNORD113-1 expression was significantly downregulated in HCC tumors compared with adjacent non-tumor tissues, and downregulation of SNORD113-1 in HCC tumors was significantly associated with worse survival of patients. In addition, CpG methylation at the promoter region of the SNORD113-1 gene was higher in HCC tumors than adjacent non-tumor tissues. Functionally, SNORD113-1 suppressed cancer cell growth in HepG2 and Huh7 cells and in a xenograft nude mouse model. Furthermore, SNORD113-1 inactivated the phosphorylation of ERK1/2 and SMAD2/3 in MAPK/ERK and TGF-β pathways. Conclusions: SNORD113-1 functions as a tumor suppressor role in HCC and may be important as a potential diagnostic and therapeutic target for HCC. [ABSTRACT FROM AUTHOR]
- Published
- 2014
- Full Text
- View/download PDF
15. MiR-221 accentuates IFN's anti-HCV effect by downregulating SOCS1 and SOCS3.
- Author
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Gang Xu, Fang Yang, Cui-Ling Ding, Jing Wang, Ping Zhao, Wen Wang, and Hao Ren
- Subjects
- *
MICRORNA , *HEPATITIS C virus , *LIVER cancer , *BLOOD serum analysis , *GENE expression in viruses , *CYTOKINES - Abstract
MiR-221 was reported to be upregulated and play roles in tumorigenesis of hepatitis C virus (HCV) associated hepatocellular carcinoma (HCC). However, the role of miR-221 in HCV infection remains unknown. In this study, it was found that miR-221 was upregulated in serum of HCV chronic hepatitis patients and Huh7.5.1 cells infected with HCVcc. Further studies indicated that miR-221 mimic could accentuate anti-HCV effect of IFN-α in HCVcc model, miR-221 mimic could further repressed 10% HCV RNA expression and 35-42% HCV core or NS5A protein expression in HCVcc infected Huh7.5.1 cells treated with 100 IU/mL IFN-α, and miR-221 inhibitor resulted in the reverse effects. Furthermore, two members of suppressor of cytokine signaling (SOCS) family, SOCS1 and SOCS3, which are well established inhibitory factors on IFN/JAK/STAT pathway, were identified as the targets of miR-221 and were involved in the effect of miR-221. In conclusion, miR-221 could accentuate IFN's anti-HCV effect by targeting SOCS1 and SOCS3. [ABSTRACT FROM AUTHOR]
- Published
- 2014
- Full Text
- View/download PDF
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