Molecular Cloning and Bioinformatic Analysis of SPATA4 Gene

Liu, Shang-Feng,Ai, Chao,Ge, Zhong-Qi,Liu, Hai-Luo,Liu, Bo-Wen,He, Shan,Wang, Zhao Korean Society for Biochemistry and Molecular Biol 2005 Journal of biochemistry and molecular biology Vol.38 No.6

Full-length cDNA sequences of four novel SPATA4 genes in chimpanzee, cow, chicken and ascidian were identified by bioinformatic analysis using mouse or human SPATA4 cDNA fragment as electronic probe. All these genes have 6 exons and have similar protein molecular weight and do not localize in sex chromosome. The mouse SPATA4 sequence is identified as significantly changed in cryptorchidism, which shares no significant homology with any known protein in swissprot databases except for the homologous genes in various vertebrates. Our searching results showed that all SPATA4 proteins have a putative conserved domain DUF1042. The percentages of putative SPATA4 protein sequence identity ranging from 30% to 99%. The high similarity was also found in 1 kb promoter regions of human, mouse and rat SPATA4 gene. The similarities of the sequences upstream of SPATA4 promoter also have a high proportion. The results of searching SymAtlas (http://symatlas.gnf.org/SymAtlas/) showed that human SPATA4 has a high expression in testis, especially in testis interstitial, leydig cell, seminiferous tubule and germ cell. Mouse SPATA4 was observed exclusively in adult mouse testis and almost no signal was detected in other tissues. The pI values of the protein are negative, ranging from 9.44 to 10.15. The subcellular location of the protein is usually in the nucleus. And the signal peptide possibilities for SPATA4 are always zero. Using the SNPs data in NCBI, we found 33 SNPs in human SPATA4 gene genomic DNA region, with the distribution of 29 SNPs in the introns. CpG island searching gives the data about CpG island, which shows that the regions of the CpG island have a high similarity with each other, though the length of the CpG island is different from each other.This research is a fundamental work in the fields of the bioinformational analysis, and also put forward a new way for the bioinformatic analysis of other genes.

Molecular Cloning and Bioinformatic Analysis of SPATA4 Gene

Shang Feng Liu,Chao Ai,Zhong Qi Ge,Hai Luo Liu,Bo Wen Liu,Shan He,Zhao Wang 한국생활환경학회 2005 BMB Reports Vol.38 No.6

Circular RNA ROCK1, a novel circRNA, suppresses osteosarcoma proliferation and migration via altering the miR-532-5p/PTEN axis

Liu Yize,Qiu Guanzhen,Luo Yinzhou,Li Shanshan,Xu Yeqiu,Zhang Yuanzhuang,Hu Jiayuan,Li Peifeng,Pan Hai,Wang Yong 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-

As the most prevalent bone tumor in children and adolescents, the pathogenesis and metastasis of osteosarcoma (OS) remain largely unclear. Here, we investigated the expression and function of a novel circular RNA (circRNA), circROCK1-E3/E4, which is back-spliced from exons 3 and 4 of Rho-associated coiled-coil containing protein kinase 1 (ROCK1) in OS. We found that circROCK1-E3/E4, regulated by the well-known RNA-binding protein quaking (QKI), was downregulated in OS and correlated with unfavorable clinical features of patients with OS. Functional proliferation and cell motility assays indicated that circROCK1-E3/E4 serves as a tumor suppressor in OS cells. Mechanistically, circROCK1-E3/E4 suppressed proliferation and migration by upregulating phosphatase and tensin homolog (PTEN) through microRNA-532-5p (miR-532-5p) sponging. In the constructed nude mouse model, circROCK1-E3/E4 inhibited tumor growth and lung metastasis in vivo. This study demonstrates the functions and molecular mechanisms of circROCK1-E3/E4 in the progression of OS. These findings may identify novel targets for the molecular therapy of OS.

Analysis of Key Genes and Pathways Associated with Colorectal Cancer with Microarray Technology

Liu, Yan-Jun,Zhang, Shu,Hou, Kang,Li, Yun-Tao,Liu, Zhan,Ren, Hai-Liang,Luo, Dan,Li, Shi-Hong Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.3

Objective: Microarray data were analyzed to explore key genes and their functions in progression of colorectal cancer (CRC). Methods: Two microarray data sets were downloaded from Gene Expression Omnibus (GEO) database and differentially expressed genes (DEGs) were identified using corresponding packages of R. Functional enrichment analysis was performed with DAVID tools to uncover their biological functions. Results: 631 and 590 DEGs were obtained from the two data sets, respectively. A total of 32 common DEGs were then screened out with the rank product method. The significantly enriched GO terms included inflammatory response, response to wounding and response to drugs. Two interleukin-related domains were revealed in the domain analysis. KEGG pathway enrichment analysis showed that the PPAR signaling pathway and the renin-angiotensin system were enriched in the DEGs. Conclusions: Our study to systemically characterize gene expression changes in CRC with microarray technology revealed changes in a range of key genes, pathways and function modules. Their utility in diagnosis and treatment now require exploration.

Roles of Signaling Pathways in the Epithelial-Mesenchymal Transition in Cancer

Liu, Xia,Yun, Fen,Shi, Lin,Li, Zhe-Hai,Luo, Nian-Rong,Jia, Yong-Feng Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.15

The epithelial-mesenchymal transition (EMT) is a cellular process though which an epithelial phenotype can be converted into a phenotype of mesenchymal cells. Under physiological conditions EMT is important for embryogenesis, organ development, wound repair and tissue remodeling. However, EMT may also be activated under pathologic conditions, especially in carcinogenesis and metastatic progression. Major signaling pathways involved in EMT include transforming growth factor ${\beta}(TGF-{\beta})$, Wnt, Notch, Hedgehog and other signaling pathways. These pathways are related to several transcription factors, including Twist, Smads and zinc finger proteins snail and slug. These interact with each other to provide crosstalk between the relevant signaling pathways. This review lays emphasis on studying the relationship between EMT and signaling pathways in carcinogenesis and metastatic progression.

IL-33 promotes IL-10 production in macrophages: a role for IL-33 in macrophage foam cell formation

Hai-Feng Zhang,Mao-Xiong Wu,Yong-Qing Lin,Shuang-Lun Xie,Tu-Cheng Huang,Pin-Ming Liu,Ru-Qiong Nie,Qin-Qi Meng,Nian-Sang Luo,Yang-Xin Chen,Jing-Feng Wang 생화학분자생물학회 2017 Experimental and molecular medicine Vol.49 No.-

We evaluated the role of IL-10- in IL-33-mediated cholesterol reduction in macrophage-derived foam cells (MFCs) and the mechanism by which IL-33 upregulates IL-10. Serum IL-33 and IL-10 levels in coronary artery disease patients were measured. The effects of IL-33 on intra-MFC cholesterol level, IL-10, ABCA1 and CD36 expression, ERK 1/2, Sp1, STAT3 and STAT4 activation, and IL-10 promoter activity were determined. Core sequences were identified using bioinformatic analysis and sitespecific mutagenesis. The serum IL-33 levels positively correlated with those of IL-10. IL-33 decreased cellular cholesterol level and upregulated IL-10 and ABCA1 but had no effect on CD36 expression. siRNA-IL-10 partially abolished cellular cholesterol reduction and ABCA1 elevation by IL-33 but did not reverse the decreased CD36 levels. IL-33 increased IL-10 mRNA production but had little effect on its stability. IL-33 induced ERK 1/2 phosphorylation and increased the luciferase expression driven by the IL-10 promoter, with the highest extent within the − 2000 to − 1752 bp segment of the 5′-flank of the transcription start site; these effects were counteracted by U0126. IL-33 activated Sp1, STAT3 and STAT4, but only the STAT3 binding site was predicted in the above segment. Site-directed mutagenesis of the predicted STAT3-binding sites (CTGCTTCCTGGCAGCAGAA→CTGCCTGGCAGCAGAA) reduced luciferase activity, and a STAT3 inhibitor blocked the regulatory effects of IL-33 on IL-10 expression. Chromatin immunoprecipitation (CHIP) confirmed the STAT3-binding sequences within the − 1997 to − 1700 and − 1091 to − 811 bp locus regions. IL-33 increased IL-10 expression in MFCs via activating ERK 1/2 and STAT3, which subsequently promoted IL-10 transcription and thus contributed to the beneficial effects of IL-33 on MFCs.

Drug-induced hyperglycaemia and diabetes: pharmacogenomics perspectives

Mou-Ze Liu,Hai-Yan He,Jian-Quan Luo,Fa-Zhong He,Zhang-Ren Chen,Yi-Ping Liu,Da-Xiong Xiang,Hong-Hao Zhou,Wei Zhang 대한약학회 2018 Archives of Pharmacal Research Vol.41 No.7

Drug-induced diabetes is widely reported inclinical conditions, and it is becoming a global issuebecause of its potential to increase the risk of severe cardiovascularcomplications. However, which drug mechanismsexert their diabetogenic effects and why the effectspresent significant inter-individual differences remain largelyunknown. Pharmacogenomics, which is the study ofhow genomic variation influences drug responses, providesan explanation for individual differences in drug-induceddiabetes. We highlight that pharmacogenomics can beinvolved in regulating the expression of genes in signalingpathways related to the pharmacokinetics or pharmacodynamicsof drugs or the pathogenesis of diabetes, contributingto the differences in drug-induced glucoseimpairment. The pharmacogenomics studies of the majordiabetogenic drugs are reviewed, including calcineurininhibitors, antipsychotics, hormones, and antihypertensivedrugs. We intend to elucidate the genetic basis of druginduceddiabetes and pave the way for the precise use ofthese drugs in the clinic.

Hypermethylation-mediated silencing of NDRG4 promotes pancreatic ductal adenocarcinoma by regulating mitochondrial function

( Hao-hong Shi ),( Hai-e Liu ),( Xing-jing Luo ) 생화학분자생물학회(구 한국생화학분자생물학회) 2020 BMB Reports Vol.53 No.12

The N-myc downstream regulated gene (NDRG) family members are dysregulated in several tumors. Functionally, NDRGs play an important role in the malignant progression of cancer cells. However, little is known about the potential implications of NDRG4 in pancreatic ductal adenocarcinoma (PDAC). The aim of the current study was to elucidate the expression pattern of NDRG4 in PDAC and evaluate its potential cellular biological effects. Here, we firstly report that epigenetic-mediated silencing of NDRG4 promotes PDAC by regulating mitochondrial function. Data mining demonstrated that NDRG4 was significantly down-regulated in PDAC tissues and cells. PDAC patients with low NDRG4 expression showed poor prognosis. Epigenetic regulation by DNA methylation was closely associated with NDRG4 down-regulation. NDRG4 overexpression dramatically suppressed PDAC cell growth and metastasis. Further functional analysis demonstrated that up-regulated NDRG4 in SW1990 and Canpan1 cells resulted in attenuated mitochondrial function, including reduced ATP production, decreased mitochondrial membrane potential, and increased fragmented mitochondria. However, opposite results were obtained for HPNE cells with NDRG4 knockdown. These results indicate that hypermethylation-driven silencing of NDRG4 can promote PDAC by regulating mitochondrial function and that NDRG4 could be as a potential biomarker for PDAC patients. [BMB Reports 2020; 53(12): 658-663]

A Novel Method of Reducing the Cogging Torque in SPM Machine with Segmented Stator

Jing, Li-Bing,Liu, Lin,Qu, Rong-Hai,Gao, Qi-Xing,Luo, Zheng-Hao The Korean Institute of Electrical Engineers 2017 Journal of Electrical Engineering & Technology Vol.12 No.2

The method of stator segmentation is generally taken to enhance the electromagnetic performance of surface-mounted permanent magnet (SPM) machine and reduce its production cost. Based on the model with single slot, the expressions of cogging torque in machine with uniform or non-uniform segmentations are deduced and the optimal combination is given. Moreover, this paper discusses a structured skewing method and put forward a novel stator structure model to reduce the cogging torque in segmented permanent magnet machine. The model can reduce the cogging torque amplitude by shifting a proper angle of slot-opening. The shifting angle formula for analysis can also be suitable for other permanent machine with segmented stator. Finally the results of finite element simulation are given to prove that the method is effective and feasible.

A Novel Method of Reducing the Cogging Torque in SPM Machine with Segmented Stator

Li-Bing Jing,Lin Liu,Rong-Hai Qu,Qi-Xing Gao,Zheng-Hao Luo 대한전기학회 2017 Journal of Electrical Engineering & Technology Vol.12 No.2

The method of stator segmentation is generally taken to enhance the electromagnetic performance of surface-mounted permanent magnet (SPM) machine and reduce its production cost. Based on the model with single slot, the expressions of cogging torque in machine with uniform or non-uniform segmentations are deduced and the optimal combination is given. Moreover, this paper discusses a structured skewing method and put forward a novel stator structure model to reduce the cogging torque in segmented permanent magnet machine. The model can reduce the cogging torque amplitude by shifting a proper angle of slot-opening. The shifting angle formula for analysis can also be suitable for other permanent machine with segmented stator. Finally the results of finite element simulation are given to prove that the method is effective and feasible.