Yunnan Red Pear-Yunhongli No.1 (YH-1)

Qun Shu,Minghua Qiu,Penglin Wang,Menglin Tong 한국원예학회 2006 한국원예학회 기타간행물 Vol.- No.-

MiR-675 Promotes the Growth of Hepatocellular Carcinoma Cells Through Cdc25A Pathway

Yu, Ya-Qun,Weng, Jun,Li, Shu-Qun,Li, Bo,Lv, Jun Asian Pacific Journal of Cancer Prevention 2016 Asian Pacific journal of cancer prevention Vol.17 No.8

Background: MicroRNAs (miRNAs) have fundamental roles in tumorigenesis. MiR-675 is upregulated in hepatocellular carcinoma(HCC) cells. However, the roles of miR-675 in hepatocellular carcinogenesis are still not fully elucidated. In this study, we focus on investigating the effect and mechanism of miR-675 in proliferation of HCC cells. Materials and Methods: The cell proliferation was measured by MTT assays after transfection with miR-675 inhibitor and miR-675 mimics in HCC cells. The expression level of miR-675 was detected by real-time quantitative reverse transcription polymerase chain reaction. Protein expression of Cdc25A was measured by western blotting analysis. Results: In MTT assays, overexpression of miR-675 promoted the proliferation of HCC cells(P<0.05. at 48 hours, P<0.01. at 72 hours) compared with the miR-675mimics control group. Downexpression of miR-675 inhibited the proliferation of HCC cells(P<0.05. at 48 hours, P<0.01. at 72 hours) compared with the miR-675inhibitor control group. In western blotting analysis, the expression level of Cdc25A was significantly increased (p<0.05) after treatment with miR-675 mimics. The expression level of Cdc25A was significantly decreased (p<0.05) after treatment with miR-675 inhibitor. Conclusions: Our results indicate that miR-675 promotes the proliferation in human hepatocellular carcinoma cells by associating with Cdc25A signaling pathway.

Optimizing Preparation Conditions for Angiotensin-I-Converting Enzyme Inhibitory Peptides Derived from Enzymatic Hydrolysates of Ovalbumin

Qun Huang,Shu-gang Li,Hui Teng,Yong-guo Jin,Mei-hu Ma,Hong-bo Song 한국식품과학회 2015 Food Science and Biotechnology Vol.24 No.6

Angiotensin-I-converting enzyme (ACE) inhibitory peptides were prepared from ovalbumin using enzyme hydrolysis with pepsin as an enzyme source. Effects of pH, enzyme dosage, substrate concentration, hydrolysis temperature, and time on the degree of hydrolysis and the ACE inhibition rate were investigated using single factor experiments. Preparation conditions for ACE inhibitory peptides were optimized using a response surface design on the base of single factor experiments. Optimum preparation conditions were a substrate concentration of 5.2 g/100 mL of D.W with a pH value of 2.5, an enzyme dosage of 14,000 U/g, and a hydrolysis time of 250 min at 30℃. The ACE inhibition rate was up to 70.55±1.13% under these conditions.

Zearalenone regulates key factors of the Kelch-like erythroid cell-derived protein with CNC homology-associated protein 1-nuclear factor erythroid 2-related factor 2 signaling pathway in duodenum of post-weaning gilts

Cheng, Qun,Jiang, Shu zhen,Huang, Li bo,Yang, Wei ren,Yang, Zai bin Asian Australasian Association of Animal Productio 2021 Animal Bioscience Vol.34 No.8

Objective: This study explored the mechanism of the Kelch-like erythroid cell-derived protein with CNC homology-associated protein 1 (Keap1)-nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway under conditions of zearalenone (ZEA)-induced oxidative stress in the duodenum of post-weaning gilts. Methods: Forty post-weaning gilts were randomly allocated to four groups and fed diets supplemented with 0, 0.5, 1.0, or 1.5 mg/kg ZEA. Results: The results showed significant reductions in the activity of the antioxidant enzymes total superoxide dismutase and glutathione peroxidase and increases the malondialdehyde content with increasing concentrations of dietary ZEA. Immunohistochemical analysis supported these findings by showing a significantly increased expression of Nrf2 and glutathione peroxidase 1 (GPX1) with increasing concentrations of ZEA. The relative mRNA and protein expression of Nrf2, GPX1 increased linearly (p<0.05) and quadratically (p<0.05), which was consistent with the immunohistochemical results. The relative mRNA expression of Keap1 decreased linearly (p<0.05) and quadratically (p<0.05) in the duodenum as the ZEA concentration increased in the diet. The relative mRNA expression of modifier subunit of glutamate-cysteine ligase (GCLM) increased quadratically (p<0.05) in all ZEA treatment groups and the relative mRNA expression of quinone oxidoreductase 1 (NQO1) catalytic subunit of glutamate-cysteine ligase decreased linearly (p<0.05) and quadratically (p<0.05) in the ZEA1.0 group and ZEA1.5 group. The relative protein expression of Keap1 and GCLM decreased quadratically (p<0.05) in the duodenum as the ZEA concentration increased in the diet, respectively. The relative protein expression of NQO1 increased linearly (p<0.05) and quadratically (p<0.05) in all ZEA treatment groups in the duodenum. Conclusion: These findings suggest that ZEA regulates the expression of key factors of the Keap1-Nrf2 signaling pathway in the duodenum, which enables resistance to ZEA-induced oxidative stress. Further studies are needed to examine the effects of ZEA induced oxidative stress on other tissues and organs in post-weaning gilts.

Histone Deacetylase Inhibitor Trichostatin A Enhances Antitumor Effects of Docetaxel or Erlotinib in A549 Cell Line

Zhang, Qun-Cheng,Jiang, Shu-Juan,Zhang, Song,Ma, Xiao-Bin Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.7

Background and Objective: Histone deacetylase (HDAC) inhibitors represent a promising class of potential anticancer agents for treatment of human malignancies. In this study, we investigated the effect of trichostatin A (TSA), one such HDAC inhibitor, in combination with docetaxel (TXT), a cytotoxic chemotherapy agent or erlotinib, a novel molecular target therapy drug, on lung cancer A549 cells. Methods: A549 cells were treated with TXT, erlotinib alone or in combination with TSA, respectively. Cell viability, apoptosis, and cell cycle distribution were evaluated using MTT (3- (4, 5-dimethylthiazol-2-yl) -2, 5-diphenyltetrazolium bromide) assay, Hochst33258 staining and flow cytometry. Moreover, immunofluorescent staining and Western blot analysis were employed to examine alterations of ${\alpha}$-tubulin, heat shock protein 90 (hsp90), epidermal growth factor receptor (EGFR), and caspase-3 in response to the different exogenous stimuli. Results: Compared with single-agent treatment, co-treatment of A549 cells with TSA/TXT or TSA/erlotinib synergistically inhibited cell proliferation, induced apoptosis, and caused cell cycle delay at the $G_2/M$ transition. Treatment with TSA/TXT or TSA/erlotinib led to a significant increase of cleaved caspase-3 expression, also resulting in elevated acetylation of ${\alpha}$-tubulin or hsp90 and decreased expression of EGFR, which was negatively associated with the level of acetylated hsp90. Conclusions: Synergistic anti-tumor effects are observed between TXT or erlotinib and TSA on lung cancer cells. Such combinations may provide a more effective strategy for treating human lung cancer.

Influence of Expression Plasmid of Connective Tissue Growth Factor and Tissue Inhibitor of Metalloproteinase-1 shRNA on Hepatic Precancerous Fibrosis in Rats

Zhang, Qun,Shu, Fu-li,Jiang, Yu-Feng,Huang, Xin-En Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.16

Background: In this study, influence caused by expression plasmids of connective tissue growth factor (CTGF) and tissue inhibitor of metalloproteinase-1 (TIMP-1) short hairpin RNA (shRNA) on mRNA expression of CTGF,TIMP-1,procol-${\alpha}1$ and PCIII in hepatic tissue with hepatic fibrosis, a precancerous condition, in rats is analyzed. Materials and Methods: To screen and construct shRNA expression plasimid which effectively interferes RNA targets of CTGF and TIMP-1 in rats. 50 cleaning Wistar male rats are allocated randomly at 5 different groups after precancerous fibrosis models and then injection of shRNA expression plasimids. Plasmid psiRNA-GFP-Com (CTGF and TIMP-1 included), psiRNA-GFP-CTGF, psiRNA-GFP-TIMP-1 and psiRNA-DUO-GFPzeo of blank plasmid are injected at group A, B, C and D, respectively, and as model control group that none plasimid is injected at group E. In 2 weeks after last injection, to hepatic tissue at different groups, protein expression of CTGF, TIMP-1, procol-${\alpha}1$ and PC III is tested by immunohistochemical method and,mRNA expression of CTGF,TIMP-1,procol-${\alpha}1$ and PCIII is measured by real-time PCR. One-way ANOVA is used to comparison between-groups. Results: Compared with model group, there is no obvious difference of mRNA expression among CTGF,TIMP-1,procol-${\alpha}1$, PC III and of protein expression among CTGF, TIMP-1, procol-${\alpha}1$, PC III in hepatic tissue at group injected with blank plasmid. Expression quantity of mRNA of CTGF, TIMP-1, procol-${\alpha}1$ and PCIII at group A, B and C decreases, protein expression of CTGF, TIMP-1, procol-${\alpha}1$, PC III in hepatic tissue is lower, where the inhibition of combination RNA interference group (group A) on procol-${\alpha}1$ mRNA transcription and procol-${\alpha}1$ protein expression is superior to that of single interference group (group B and C) (P<0.01 or P<0.05). Conclusions: RNA interference on CTGF and/or TIMP-1 is obviously a inhibiting factor for mRNA and protein expression of CTGF, TIMP-1, procol-${\alpha}1$ and PCIII. Combination RNA interference on genes of CTGF and TIMP-1 is superior to that of single RNA interference, and this could be a contribution for prevention of precancerous condition.

The Suppression of Radio Interference in HF Radar

Chen Zhi Qun,Zhao Shu Qin,Quan Tai Fan 대한전자공학회 1998 ICEIC:International Conference on Electronics, Inf Vol.1 No.1

The 2518 A/G Polymorphism in the MCP-1 Gene and Cancer Risk: A Meta-analysis

Jia, Liu-Qun,Shen, Yong-Chun,Guo, Shu-Jin,Hu, Qian-Jing,Pang, Cai-Shuang,Wang, Tao,Chen, Lei,Wen, Fu-Qiang Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.6

Background: The 2518 A/G polymorphism in the MCP-1 gene has been extensively studied for association swith cancer; however, results from replication studies have been inconsistent. The aim of this investigation was to determine links with risk of cancer by meta-analysis. Methods: We searched Pubmed, Embase, CNKI, Weipu and Wanfang databases, covering all case-control studies until March, 2013. Statistical analyses were performed using the Revman 5.0 software. Results: A total of 11 case-control studies met our inclusion criteria, including 1,422 cases and 2,237 controls. The results indicated that the MCP-1 2518 gene polymorphism had no association with cancer risk overall (GG vs.GA+ AA: OR = 0.89, 95%CI = 0.61-1.28, P = 0.52). However, in the subgroup analysis by ethnicity, a decrease of cancer risk was found in Asian populations (GG vs.GA+ AA: OR = 0.79, 95%CI = 0.63-0.99, P = 0.04). Conclusion: This meta-analysis suggested that the 2518A/G polymorphism of MCP-1 gene is associated with risk of cancer among Asian, but not in Caucasian populations.

Predictive Significance of Claudin-3 for Epithelial Barrier Dysfunction in Chronic Rhinosinusitis With Nasal Polyps

Huang Zhi-Qun,Ye Jing,Liu Jing,Sun Li-Ying,Ong Hsiao Hui,Wei Yong-Hao,Fu Shu-Cai,Hu Xiao-Xun,Xu Yu,Wang De-Yun 대한천식알레르기학회 2023 Allergy, Asthma & Immunology Research Vol.15 No.4

Purpose: The abnormal expression of tight junction (TJ) plays a vital role in the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP). However, there is no appropriate tool to distinguish and diagnose epithelial barrier defects in clinical practice. This study aimed to evaluate the predictive value of claudin-3 for epithelial barrier dysfunction in CRSwNP. Methods: In this study, TJ protein levels were evaluated by real-time quantitative polymerase chain reaction, immunofluorescent, and immunohistochemistry staining in control subjects and CRSwNP patients. The receiver operating characteristic (ROC) curve was created to assess the predictive value of TJ breakdown in clinical outcomes. In vitro, human nasal epithelial cells were cultured at the air-liquid interface to analyze the transepithelial electrical resistance (TER) level. Results: The expression levels of occludin, tricellulin, claudin-3, and claudin-10 were decreased (all P < 0.05), and those of claudin-1 was increased (P < 0.05) in CRSwNP patients as compared to healthy subjects. Additionally, claudin-3 and occludin levels were negatively correlated with the computed tomography score in CRSwNP (all P < 0.05), and the ROC curve indicated that the claudin-3 level had the most predictive accuracy in evaluating epithelial barrier disruption (area under the curve = 0.791, P < 0.001). Finally, the time-series analysis showed the highest correlation coefficient between TER and claudin-3 (cross-correlation function = 0.75). Conclusion: In this study, we suggest that claudin-3 could be a valuable biomarker for predicting nasal epithelial barrier defects and disease severity in CRSwNP.

Aflatoxin B1 Promotes Cell Growth and Invasion in Hepatocellular Carcinoma HepG2 Cells through H19 and E2F1

Lv, Jun,Yu, Ya-Qun,Li, Shu-Qun,Luo, Liang,Wang, Qian Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.6

H19 is an imprinted oncofetal gene, and loss of imprinting at the H19 locus results in over-expression of H19 in cancers. Aflatoxin B1(AFB1) is regarded as one of the most dangerous carcinogens. Exposure to AFB1 would most easily increase susceptibility to diseases such as hepatocellular carcinoma(HCC) but any possible relationship between AFB1 and H19 is not clear. In present study, we found that AFB1 could up-regulate the expression of H19 and promote cell growth and invasion by hepatocellular carcinoma HepG2 cells. Knocking down H19 RNA co ld reverse the effects of AFB1 on cell growth and invasion. In addition, AFB1 induced the expression of E2F1 and its knock-down could down-regulate H19 expression and suppress cell growth and invasion in hepatocellular carcinoma HepG2 cells. Furthermore, E2F1 over-expression could up-regulate H19 expression and promote cell growth and invasion, with binding to the H19 promoter being demonstrated by chromatin immunoprecipitation assays (ChIP). In summary, our results suggested that aflatoxin B1could promote cell growth and invasion in hepatocellular carcinoma HepG2 cells through actions on H19 and E2F1.