A Review on Microbial Decaffeination

Hui-Shi Wu,Xin-Qiang Zheng,Yue-Rong Liang,Jian-Hui Ye,Jian-Liang Lu 한국차학회 2015 한국차학회지 Vol.- No.S

Exclusive exposure of caffeine might bring some adverse effects to human health, and cause some risks to environment. Microbial decaffeination might be a new alternative approach because of its high specificity and efficiency. Many studies revealed that several microorganisms can degrade caffeine, including genera Alcaligenes,Rhodococcus, Klebsiella, Acinetobacter, Enterobacter, Stenotrophomonas and Pseudomonas. Biodegradation of caffeine can be significantly influenced by temperature, pH, aeration rate and initial caffeine concentration of the incubation. There are two main pathways of caffeine biodegradation: C-8 oxidation and N-demethylation, while N-demethylation is the general catabolism pathway in bacteria. Application of microbial decaffeination has also been discussed in this review.

No Association Between Tea Consumption and Risk of Renal Cell Carcinoma: A Meta-analysis of Epidemiological Studies

Hu, Zheng-Hui,Lin, Yi-Wei,Xu, Xin,Chen, Hong,Mao, Ye-Qing,Wu, Jian,Xu, Xiang-Lai,Zhu, Yi,Li, Shi-Qi,Zheng, Xiang-Yi,Xie, Li-Ping Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.3

Objective: To evaluate the association between tea consumption and the risk of renal cell carcinoma. Methods: We searched PubMed, Web of Science and Scopus between 1970 and November 2012. Two evaluators independently reviewed and selected articles based on predetermined selection criteria. Results: Twelve epidemiological studies (ten case-control studies and two cohort studies) were included in the final analysis. In a meta-analysis of all included studies, when compared with the lowest level of tea consumption, the overall relative risk (RR) of renal cell carcinoma for the highest level of tea consumption was 1.03 (95% confidence interval [CI] 0.89-1.21). In subgroup meta-analyses by study design, there was no significant association between tea consumption and renal cell carcinoma risk in ten case-control studies using adjusted data (RR=1.08, 95% CI 0.84-1.40). Furthermore, there was no significant association in two cohort studies using adjusted data (RR=0.95, 95% CI 0.81-1.12). Conclusion: Our findings do not support the conclusion that tea consumption is related to decreased risk of renal cell carcinoma. Further prospective cohort studies are required.

Gene Expression Profiles of HeLa Cells Impacted by Hepatitis C Virus Non-structural Protein NS4B

Zheng, Yi,Ye, Lin-Bai,Liu, Jing,Jing, Wei,Timani, Khalid A.,Yang, Xiao-Jun,Yang, Fan,Wang, Wei,Gao, Bo,Wu, Zhen-Hui Korean Society for Biochemistry and Molecular Biol 2005 Journal of biochemistry and molecular biology Vol.38 No.2

By a cDNA array representing 2308 signal transduction related genes, we studied the expression profiles of HeLa cells stably transfected by Hepatitis C virus nonstructural protein 4B (HCV-NS4B). The alterations of the expression of four genes were confirmed by real-time quantitative RT-PCR; and the aldo-keto reductase family 1, member C1 (AKR1C1) enzyme activity was detected in HCV-NS4B transiently transfected HeLa cells and Huh-7, a human hepatoma cell line. Of the 2,308 genes we examined, 34 were up-regulated and 56 were down-regulated. These 90 genes involved oncogenes, tumor suppressors, cell receptors, complements, adhesions, transcription and translation, cytoskeletion and cellular stress. The expression profiling suggested that multiple regulatory pathways were affected by HCV-NS4B directly or indirectly. And since these genes are related to carcinogenesis, host defense system and cell homeostatic mechanism, we can conclude that HCV-NS4B could play some important roles in the pathogenesis mechanism of HCV.

Centromere protein N promotes lung adenocarcinoma progression by activating PI3K/AKT signaling pathway

Zheng Yi,You Hui,Duan Jingzhu,Chen Biyu,Wu Chenlin,Chen Peipei,Wang Meifang 한국유전학회 2022 Genes & Genomics Vol.44 No.9

Background: As an important member of centromere family, centromere associated protein N (CENPN) was abnormally expressed in varied malignant tumors. Objective: This paper aimed to analyze the expression and related mechanism of CENPN in lung adenocarcinoma (LUAD). Methods: The expression of CENPN in LUAD was analyzed by Gene Expression Profiling Interactive Analysis (GEPIA) database. The mRNA expression, protein expression, cell viability, cell invasion, cell apoptosis, cell stem like characteristics were detected by RT-PCR, western blot, CCK8 assay, transwell assay, flow cytometry and spheroidization assay, respectively. Finally, the pathological changes of xenograft were estimated by H&E staining, and the expression of proteins was detected by immunohistochemistry. Results: GEPIA analysis showed that the CENPN expression in LUAD was significantly higher than that in normal lung tissue, which was negatively correlated with the prognosis. These results were consistent with our clinical data. Besides, CENPN was highly expressed in LUAD cell lines. In addition, the upregulation of CENPN amplified the cell viability, stemness and invasive ability in PC9 cells. However, the knockdown of CENPN inhibited the cell activity, stemness, invasive ability with increased cell apoptosis in A549. Furthermore, CENPN could positively regulate the phosphorylation of PI3K and AKT. The PI3K inhibitor, 740Y-P, could reverse the effect of CENPN silencing on the expression of Ki-67, cleaved caspase 3, OCT4, and snail 1. Finally, the downregulation of CENPN restrained the growth of xenograft and inactivated the PI3K/AKT pathway. Conclusion: CENPN was abnormally overexpressed in LUAD, and promoted tumor progression of LUAD by affecting PI3K/AKT pathway.

Effect of Tea Polyphenols on the Adhesion of Highly Metastatic Human Lung Carcinoma Cell Lines to Endothelial Cells in Vitro

Zheng, Feng-Jin,Shi, Lin,Yang, Jun,Deng, Xiao-Hui,Wu, Yu-Quan,Yan, Xi-Qing,Huang, Ning Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.8

Aim: Tea polyphenols are known to play roles in critical steps of human lung carcinoma cell metastasis. For understanding the mechanisms whereby they inhibit tumor metastasis, the present study was conducted to investigate their effects on the adhesion of highly metastatic lung carcinoma cell lines (PG cells) to endothelial cells (EC cells) and adhesion molecule expression in vitro. Methods: The expression of CD44 or CD54 in the PG cells was detected by flow cytometry and adhesion of PG cells to EC cells was assessed by confocal microscopy double fluorescence staining. Results: The results showed that tea polyphenols: (1) inhibited the expression of CD44 and CD54, two important adhesion molecules in the PG cells in a dose-dependent manner; (2) significantly blocked the adhesion of PG cells to EC cells not only in a state of rest but also when active; and (3) influenced CD44 and CD54 expression during the adhesion process of PG cells to EC cells. Conclusions: The data indicated that the blocking role of tea polyphenols in the adhesion of PG cells to EC cells is related to CD44 and CD54. The mechanism of tea polyphenol prevention of human lung carcinoma metastasis might be through inhibiting adhesion molecule expression to block cancer cell adhesion.

Genetic Polymorphisms of Glutathione S-transferase M1 and Prostate Cancer Risk in Asians: A Meta-analysis of 18 Studies

Hu, Zheng-Hui,Lin, Yi-Wei,Xu, Xin,Chen, Hong,Mao, Ye-Qing,Wu, Jian,Zhu, Yi,Xu, Xiang-Lai,Xie, Li-Ping Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.1

Background: Many studies have investigated associations between the glutathione S-transferase M1 (GSTM1) null polymorphism and risk of prostate cancer, but the impact of GSTM1 in people who live in Asian countries is still unclear owing to inconsistencies across results. Methods: We searched the PubMed, Web of Science, Scopus, Ovid and CNKI databases for studies of associations between the GSTM1 null genotype and risk of prostate cancer in people who live in Asian countries, and estimated summary odds ratios (ORs) with 95% confidence intervals (95% CIs). Results: A total of 18 case-control studies with 2,172 cases and 3,258 controls were included in this meta-analysis, which showed the GSTM1 null genotype to be significantly associated with increased risk of prostate cancer in people who live in Asian countries (random-effects OR=1.74, 95% CI1.44-2.09, P<0.001). Similar results were found in East Asians (OR=1.41; 95% CI: 1.12-1.78; P=0.004) and Caucasians in Asia (OR=2.19; 95% CI: 1.85-2.60; P<0.001). No evidence of publication bias was observed. Conclusions: This meta-analysis of available data suggested that the GSTM1 null genotype does contribute to increased risk of prostate cancer in people who live in Asian countries.

Growth and Differentiation Effects of Homer3 on a Leukemia Cell Line

Li, Zheng,Qiu, Hui-Ying,Jiao, Yang,Cen, Jian-Nong,Fu, Chun-Mei,Hu, Shao-Yan,Zhu, Ming-Qing,Wu, De-Pei,Qi, Xiao-Fei Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.4

The Homer protein family, also known as the family of cytoplasmic scaffolding proteins, which include three subtypes (Homer1, Homer2, Homer3). Homer3 can regulate transcription and play a very important role in the differentiation and development for some tissues (e.g. muscle and nervous systems). The current studies showed that Homer3 abnormal expression changes in acute myeloid leukemia (AML). Forced expression of Homer3 in transfected K562 cells inhibited proliferation, influenced the cell cycle profile, affected apoptosis induced by $As_2O_3$ through inhibition of Bcl2 expression, and also promoted cell differentiation induced by 12-O-tetra decanoylphorbol-acetate (TPA). These results showed that Homer3 is a novel gene which plays a certain role in the occurrence and development of AML.

Inhibition of Fatty Acid β-Oxidation by Fatty Acid Binding Protein 4 Induces Ferroptosis in HK2 Cells Under High Glucose Conditions

Zhihua Zheng,Jiasi Chen,Keping Wu,Yan Lei,Mingcheng Huang,Lokyu Cheng,Hui Guan,Jiawen Lin,Ming Zhong,Xiaohua Wang 대한내분비학회 2023 Endocrinology and metabolism Vol.38 No.2

Background: Ferroptosis, which is caused by an iron-dependent accumulation of lipid hydroperoxides, is a type of cell death linked todiabetic kidney disease (DKD). Previous research has shown that fatty acid binding protein 4 (FABP4) is involved in the regulation of ferroptosis in diabetic retinopathy. The present study was constructed to explore the role of FABP4 in the regulation of ferroptosis in DKD. Methods: We first detected the expression of FABP4 and proteins related to ferroptosis in renal biopsies of patients with DKD. Then, we used a FABP4 inhibitor and small interfering RNA to investigate the role of FABP4 in ferroptosis induced by high glucosein human renal proximal tubular epithelial (HG-HK2) cells. Results: In kidney biopsies of DKD patients, the expression of FABP4 was elevated, whereas carnitine palmitoyltransferase-1A (CPT1A), glutathione peroxidase 4, ferritin heavy chain, and ferritin light chain showed reduced expression. In HG-HK2 cells, the induction of ferroptosis was accompanied by an increase in FABP4. Inhibition of FABP4 in HG-HK2 cells changed the redox state, suppressing the production of reactive oxygen species, ferrous iron (Fe2+), and malondialdehyde, increasing superoxide dismutase, and reversing ferroptosis-associated mitochondrial damage. The inhibition of FABP4 also increased the expression of CPT1A, reversed lipiddeposition, and restored impaired fatty acid β-oxidation. In addition, the inhibition of CPT1A could induce ferroptosis in HK2 cells. Conclusion: Our results suggest that FABP4 mediates ferroptosis in HG-HK2 cells by inhibiting fatty acid β-oxidation.

Gene Expression Profiles of HeLa Cells Impacted by Hepatitis C Virus Non-structural Protein NS4B

( Yi Zheng ),( Lin Bai Ye ),( Jing Liu ),( Wei Jing ),( Khalid A. Timani ),( Xiao Jun Yang ),( Fan Yang ),( Wei Wang ),( Bo Gao ),( Zhen Hui Wu ) 생화학분자생물학회 2005 BMB Reports Vol.38 No.2

By a cDNA array representing 2308 signal transductionrelated genes, we studied the expression profiles of HeLa cells stably transfected by Hepatitis C virus nonstructural protein 4B (HCV-NS4B). The alterations of the expression of four genes were confirmed by real-time quantitative RT PCR; and the aldo-keto reductase family 1, member Cl (AKR1C1) enzyme activity was detected in HCV-NS4B transiently transfected HeLa cells and Huh-7, a human hepatoma cell line. Of the 2,308 genes we examined, 34 were up-regulated and 56 were down-regulated. These 90 genes involved oncogenes, tumor suppressors, cell receptors, complements, adhesions, transcription and translation, cytoskeletion and cellular stress. The expression profiling suggested that multiple regulatory pathways were affected by HCV-NS4B directly or indirectly. And since these genes are related to carcinogenesis, host defense system and cell homeostatic mechanism, we can conclude that HCV-NS4B could play some important roles in the pathogenesis mechanism of HCV.

Ubiquitination of p53 is Involved in Troglitazone Induced Apoptosis in Cervical Cancer Cells

Chen, Hui-Min,Zhang, Ding-Guo,Wu, Jin-Xiz,Pei, Dong-Sheng,Zheng, Jun-Nian Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.5

Peroxisome proliferator-activated receptor gamma (PPAR-${\gamma}$), a ligand-dependent nuclear transcription factor, has been found to widely exist in tumor tissues and plays an important role in affecting tumor cell growth. In this study, we investigated the effect of PPAR-${\gamma}$ on aspects of the cervical cancer malignant phenotype, such as cell proliferation and apoptosis. Cell growth assay, Western blotting, Annexin V and flow cytometry analysis consistently showed that treatment with troglitazone (TGZ, a PPAR-${\gamma}$ agonist) led to dose-dependent inhibition of cervical cancer cell growth through apoptosis, whereas T0070907 (another PPAR-${\gamma}$ antagonist) had no effect on Hela cell proliferation and apoptosis. Furthermore, we also detected the protein expression of p53, p21 and Mdm2 to explain the underlying mechanism of PPAR-${\gamma}$ on cellular apoptosis. Our work, finally, demonstrated the existence of the TGZ-PPAR-${\gamma}$-p53 signaling pathway to be a critical regulator of cell apoptosis. These results suggested that PPAR-${\gamma}$ may be a potential therapeutic target for cervical cancer.