Identification of Specific Gene Modules in Mouse Lung Tissue Exposed to Cigarette Smoke

Xing, Yong-Hua,Zhang, Jun-Ling,Lu, Lu,Li, De-Guan,Wang, Yue-Ying,Huang, Song,Li, Cheng-Cheng,Zhang, Zhu-Bo,Li, Jian-Guo,Xu, Guo-Shun,Meng, Ai-Min Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.10

Background: Exposure to cigarette may affect human health and increase risk of a wide range of diseases including pulmonary diseases, such as chronic obstructive pulmonary disease (COPD), asthma, lung fibrosis and lung cancer. However, the molecular mechanisms of pathogenesis induced by cigarettes still remain obscure even with extensive studies. With systemic view, we attempted to identify the specific gene modules that might relate to injury caused by cigarette smoke and identify hub genes for potential therapeutic targets or biomarkers from specific gene modules. Materials and Methods: The dataset GSE18344 was downloaded from the Gene Expression Omnibus (GEO) and divided into mouse cigarette smoke exposure and control groups. Subsequently, weighted gene co-expression network analysis (WGCNA) was used to construct a gene co-expression network for each group and detected specific gene modules of cigarette smoke exposure by comparison. Results: A total of ten specific gene modules were identified only in the cigarette smoke exposure group but not in the control group. Seven hub genes were identified as well, including Fip1l1, Anp32a, Acsl4, Evl, Sdc1, Arap3 and Cd52. Conclusions: Specific gene modules may provide better understanding of molecular mechanisms, and hub genes are potential candidates of therapeutic targets that may possible improve development of novel treatment approaches.

Characterization of the TAK1 gene in Apis cerana cerana (AccTAK1) and its involvement in the regulation of tissue-specific development

( Fei Meng ),( Ming Jiang Kang ),( Li Liu ),( Lu Luo ),( Bao Hua Xu ),( Xing Qi Guo ) 생화학분자생물학회(구 한국생화학분자생물학회) 2011 BMB Reports Vol.44 No.3

TGF-β activated kinase-1 (TAK1) plays a pivotal role in developmental processes in many species. Previous research has mainly focused on the function of TAK1 in model organisms, and little is known about the function of TAK1 in hymenoptera insects. Here, we isolated and characterized the TAK1 gene from Apis cerana cerana. Promoter analysis of AccTAK1 revealed the presence of transcription factor binding sites related to early development. Real-time quantitative PCR and immunohistochemistry experiments revealed that AccTAK1 was expressed at high levels in fourth instar larvae, primarily in the abdomen, in the intestinal wall cells of the midgut and in the secretory cells of the salivary glands. In addition, AccTAK1 expression in fourth instar larvae could be dramatically induced by treatment with pesticides and organic solvents. These observations suggest that AccTAK1 may be involved in the regulation of early development in the larval salivary gland and midgut. [BMB reports 2011; 44(3): 187-192]

Expression patterns of five heat shock proteins in Sesamia inferens (Lepidoptera: Noctuidae) during heat stress

Xiao-Tian Tang,Meng Sun,Ming-Xing Lu,Yu-Zhou Du 한국응용곤충학회 2015 Journal of Asia-Pacific Entomology Vol.18 No.3

Heat shock proteins (HSPs) play important roles in the adaptation of organisms to environmental changes. In this study, we explore the role of HSPs during heat stress in Sesamia inferens (Walker) (Lepidoptera: Noctuidae), an important pest of rice. In order to understand themechanistic basis of ecological adaptability and stress tolerance, we analyzed the expression profiles of genes encoding five S. inferens heat shock proteins (Sihsps) across temperature gradients by real-time quantitative PCR. Our results indicated that genes encoding ribosomal protein S13 (RPS13) and β-actin (ACTB) were the most stable reference genes under high temperature stress. The mRNA levels of Sihsp19.6, Sihsp20.6 and Sihsp83 were significantly upregulated by heat stress; however, the expression of Sihsp21.4 and Sihsc70 did not vary significantly. The massive increase in the expression of Sihsp19.6 and Sihsp20.6 by thermal stress suggests a critical role in preventing cellular damage to S. inferens. Moreover, the threshold temperatures (39 °C for Sihsp19.6, Sihsp20.6 and Sihsp83)may partly explain the more southern distribution of S. inferens. Our results also support the contention that the absence of introns may favor the expression of stress-responsive genes (e.g. Sihsp19.6, Sihsp20.6 and Sihsp83 in the present study).

miR-638 Serves as a Biomarker of 5-Fluorouracil Sensitivity to Neoadjuvant Chemotherapy in Breast Cancer

Bin Wang,Kun Wang,Jian Yu,Xiao-meng Hao,Yu-lu Liu,Ai-Yan Xing 한국유방암학회 2022 Journal of breast cancer Vol.25 No.3

Purpose: Neoadjuvant chemotherapy (NAC) is widely used to treat breast cancer (BC). The prediction and evaluation of chemotherapy responses remains a significant challenge. Methods: MicroRNAs (miRNAs) play a crucial role in cancer drug resistance. We used a miRNA microarray and identified that miR-638 is downregulated in chemoresistant cases. However, the exact role of miR-638 and the underlying mechanisms of chemoresistance remain unclear. Using real-time quantitative reverse transcription polymerase chain reaction, we found significant downregulation of miR-638 in chemoresistant patients compared with chemosensitive patients. To explore the function of miR-638, we overexpressed and inhibited miR-638 expression in MDA-MB-231 and MCF-7 cells by transfecting them with miR-638 mimics and miR-638 inhibitor, respectively. Cell proliferation and apoptosis were measured using MTS and flow cytometry, respectively. A minimal patient-derived xenograft (MiniPDX™) model was established to evaluate the chemosensitivity to different drugs. Results: The results showed that cell proliferation decreased and cell apoptosis increased in cells transfected with the miR-638 mimic, and cell proliferation and apoptosis were reversed with transfection of miR-638 inhibitor compared with the control group. Among patients who received 5-fluorouracil (5-FU), miR-638 expression levels were lower in the chemoresistant group than in the chemosensitive group. The MiniPDX™ model showed that MDA-MB-231 cells overexpressing miR-638 were more susceptible to 5-FU treatment in vivo. Conclusion: We provided evidence of acquired resistance to 5-FU caused by miR-638 deficiency. Alterations in miR-638 may be used with 5-FU chemotherapy during NAC for BC.

Performance of Au/FeOx–TiO2 catalyst for liquid phase selective hydrogenation of phthalic anhydride to phthalide

Yingxin Liu,Zuojun Wei,Tiefeng Xing,Meng Lu,Xiaonian Li 한국공업화학회 2015 Journal of Industrial and Engineering Chemistry Vol.23 No.-

Gold catalysts supported on FeOx–TiO2 with various Fe2O3 contents were prepared by deposition– precipitation method and used for phthalic anhydride hydrogenation to phthalide. The effect of Fe2O3 on the physico-chemical property and the performance of Au/TiO2 were investigated. The reaction conditions were optimized. Adding 5 wt.% Fe2O3 on Au/TiO2 could enhance the activity and stability, which was contributed to the increase in the strength of the catalyst structure and the decrease in the loss of gold from catalyst. Using Au/5%FeOx–TiO2, phthalic anhydride conversion and phthalide selectivity reached 95.4% and 94.5%, respectively, at 190 8C and 3.0 MPa H2 for 7 h.

Research Progress on the Livin Gene and Osteosarcomas

Li, Cheng-Jun,Cong, Yu,Liu, Xiao-Zhou,Zhou, Xing,Shi, Xin,Wu, Su-Jia,Zhou, Guang-Xin,Lu, Meng Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.20

Osteosarcoma is a common malignant tumor of bone, but mechanisms underlying its development are still unclear. At present, it is believed that the inhibition of normal apoptotic mechanisms is one of the reasons for the development of tumors, so specific stimulation of tumor cell apoptosis can be considered as an important therapeutic method. Livin, as a member of the newly discovered inhibitor of apoptosis proteins (IAPs) family, has specifically high expression in tumor tissues and can inhibit tumor cell apoptosis through multiple ways, which can become a new target for malignant tumor treatment (including osteosarcoma) and might of great significance in the clinical diagnosis of tumors and the screening of anti-tumor agents and carcinoma treatment.

Fresh Washed Microbiota Transplantation Alters Gut Microbiota Metabolites to Ameliorate Sleeping Disorder Symptom of Autistic Children

Liu Nai-Hua,Liu Hong-Qian,Zheng Jia-Yi,Zhu Meng-Lu,Wu Li-Hao,Pan Hua-Feng,He Xing-Xiang 한국미생물학회 2023 The journal of microbiology Vol.61 No.8

Accumulating studies have raised concerns about gut dysbiosis associating autism spectrum disorder (ASD) and its related symptoms. However, the effect of gut microbiota modification on the Chinese ASD population and its underlying mechanism were still elusive. Herein, we enrolled 24 ASD children to perform the first course of fresh washed microbiota transplantation (WMT), 18 patients decided to participate the second course, 13 of which stayed to participate the third course, and there were 8 patients at the fourth course. Then we evaluated the effects of fresh WMT on these patients and their related symptoms. Our results found that the sleeping disorder symptom was positively interrelated to ASD, fresh WMT significantly alleviated ASD and its sleeping disorder and constipation symptoms. In addition, WMT stably and continuously downregulated Bacteroides/ Flavonifractor/Parasutterella while upregulated Prevotella_9 to decrease toxic metabolic production and improve detoxification by regulating glycolysis/myo-inositol/D-glucuronide/D-glucarate degradation, L-1,2-propanediol degradation, fatty acid β-oxidation. Thus, our results suggested that fresh WMT moderated gut microbiome to improve the behavioral and sleeping disorder symptoms of ASD via decrease toxic metabolic production and improve detoxification. Which thus provides a promising gut ecological strategy for ASD children and its related symptoms treatments.

Molecular characterization and inhibition analysis of the acetylcholinesterase gene from the silkworm maggot, Exorista sorbillans

( Guo Jun Lang ),( Ming Yan Zhang ),( Bao Ling Li ),( Lin Lin Yu ),( Xing Meng Lu ),( Chuan Xi Zhang ) 생화학분자생물학회 (구 한국생화학분자생물학회) 2010 BMB Reports Vol.43 No.8

Several organophosphorus (OP) insecticides can selectively kill the silkworm maggot, Exorista sorbillans (Es) (Diptera: Tachinidae), while not obviously affecting the host (Bombyx mori) larvae, but the mechanism is not yet clear. In this study, the cDNA encoding an acetylcholinesterase (AChE) from the field Es was isolated. One point mutation (Gly353Ala) was identified. The Es-353G AChE and Es-353A AChE were expressed in baculovirus- insect cell system, respectively. The inhibition results showed that for eserine and Chlorpyrifos, Es-353A AChE was significantly less sensitive than Es-353G AChE. Meanwhile, comparison of the I(50) values of eserine, dichlorvos, Chlorpyrifos and omethoate of recombinant Es AChEs with its host (Bombyx mori) AChEs indicated that, both Es AChEs are more sensitive than B. mori AChEs. The results give an insight of the mechanism that some OP insecticides can selectively kills Es while without distinct effect on its host, B. mori. [BMB reports 2010; 43(8): 573-578]

Effect of Trichostatin A on CNE2 Nasopharyngeal Carcinoma Cells - Genome-wide DNA Methylation Alteration

Yang, Xiao-Li,Zhang, Cheng-Dong,Wu, Hua-Yu,Wu, Yong-Hu,Zhang, Yue-Ning,Qin, Meng-Bin,Wu, Hua,Liu, Xiao-Chun,Lina, Xing,Lu, Shao-Ming Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.11

Trichostatin A (TSA) is a histone deacetylase (HDAC) inhibitor. We here investigated its effects on proliferation and apoptosis of the CNE2 carcinoma cell line, and attempted to establish genome-wide DNA methylation alteration due to differentially histone acetylation status. After cells were treated by TSA, the inhibitory rate of cell proliferation was examined with a CCK8 kit, and cell apoptosis was determined by flow cytometry. Compared to control, TSA inhibited CNE2 cell growth and induced apoptosis. Furthermore, TSA was found to induce genome-wide methylation alteration as assessed by genome-wide methylation array. Overall DNA methylation level of cells treated with TSA was higher than in controls. Function and pathway analysis revealed that many genes with methylation alteration were involved in key biological roles, such as apoptosis and cell proliferation. Three genes (DAP3, HSPB1 and CLDN) were independently confirmed by quantitative real-time PCR. Finally, we conclude that TSA inhibits CNE2 cell growth and induces apoptosis in vitro involving genome-wide DNA methylation alteration, so that it has promising application prospects in treatment of NPC in vivo. Although many unreported hypermethylated/hypomethylated genes should be further analyzed and validated, the pointers to new biomarkers and therapeutic strategies in the treatment of NPC should be stressed.