Development of lattice inversion modified embedded atom method and its applications

Xianbao Duan,Bing Zhou,Rong Chen,Huamin Zhou,YanweiWen,Bin Shan 한국물리학회 2014 Current Applied Physics Vol.14 No.12

The modified embedded atom method (MEAM) has been widely used in describing the physical properties of elemental crystals, alloys and compounds with multiple lattice structures. We report here the development of a reliable procedure to reduce the complexity of the MEAM formalism by removing the many-body screening function. In the proposed formulation, the interatomic pair potential is obtained by applying Chen-M€obius lattice inversion up to fifth nearest neighbors, so that the cohesive energy curve can be reproduced faithfully. The newly developed model (Lattice Inversion MEAM, LI-MEAM), which can be viewed as a direct extension of the embedded atom method (EAM), no longer requires the computation of many-body screen functions and has fewer adjustable parameters than MEAM. As an illustration, we optimized the potential parameters of body centered cubic iron (bcc-Fe). The values of the calculated physical properties agree well with experimental results. We further investigated the sizedependent melting behavior of bcc-Fe nanoparticles (NPs) with particle size ranging from 725-atom (~25 Å) to 22899-atom (~80 Å) using replica exchange molecular dynamics (REMD) simulations. Our simulations show advantages of LI-MEAM in modeling of the melting process and quantitatively reveals that the liquid skin melting (LSM) process of bcc-Fe NPs.

Analysis of Different Activation Statuses of Human Mammary Epithelial Cells from Young and Old Groups

Feng, Chen-Chen,Chen, Li-Na,Chen, Mei-Jun,Li, Wan,Jia, Xu,Zhou, Yan-Yan,He, Wei-Ming Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.8

Human mammary epithelial cells have different proliferative statuses and demonstrate a close relationship with age and cell proliferation. Research on this topic could help understand the occurrence, progression and prognosis of breast cancer. In this article, using significance analysis of a microarray algorithm, we analyzed gene expression profiles of human mammary epithelial cells of different proliferative statuses and different age groups. The results showed there were significant differences in gene expression in the same proliferation status between elderly and young groups. Three common differentially expressed genes were found to dynamically change with the proliferation status and to be closely related to tumorigenesis. We also found elderly group had less status-related differential genes from actively proliferating status to intermediate status and more statusrelated differential genes from intermediate status than the young group. Finally, functional enrichment analyses allowed evaluation of the detailed roles of these differentially-expressed genes in tumor progression.

CircFam190a: a critical positive regulator of osteoclast differentiation via enhancement of the AKT1/HSP90β complex

Chen Kun,Chen Xi,Lang Chuandong,Yuan Xingshi,Huang Junming,Li Zhi,Xu Mingyou,Wu Kerong,Zhou Chenhe,Li Qidong,Zhu Chen,Liu Lianxin,Shang Xifu 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-

The identification of key regulatory factors that control osteoclastogenesis is important. Accumulating evidence indicates that circular RNAs (circRNAs) are discrete functional entities. However, the complexities of circRNA expression as well as the extent of their regulatory functions during osteoclastogenesis have yet to be revealed. Here, based on circular RNA sequencing data, we identified a circular RNA, circFam190a, as a critical regulator of osteoclast differentiation and function. During osteoclastogenesis, circFam190a is significantly upregulated. In vitro, circFam190a enhanced osteoclast formation and function. In vivo, overexpression of circFam190a induced significant bone loss, while knockdown of circFam190a prevented pathological bone loss in an ovariectomized (OVX) mouse osteoporosis model. Mechanistically, our data suggest that circFam90a enhances the binding of AKT1 and HSP90β, promoting AKT1 stability. Altogether, our findings highlight the critical role of circFam190a as a positive regulator of osteoclastogenesis, and targeting circFam190a might be a promising therapeutic strategy for treating pathological bone loss.

IQGAP1 is overexpressed in hepatocellular carcinoma and promotes cell proliferation by Akt activation

Chen, Feng,Zhu, Hai-Hong,Zhou, Lin-Fu,Wu, Shan-Shan,Wang, Jing,Chen, Zhi Korean Society for Biochemistry and Molecular Bion 2010 Experimental and molecular medicine Vol.42 No.7

The scaffold protein IQGAP1 shows elevated levels in several cancer types, but its expression in hepatocellular carcinoma is unknown. We found that 58% of human hepatocellular carcinoma tissue samples had increased IQGAP1 expression compared to adjacent normal tissue. Overexpressing IQGAP1 raised the in vivo tumorigenicity of hepatocellular carcinoma cells, and forced overexpression of IQGAP1 in vitro stimulated cell proliferation. Cell growth was reduced by knockdown or mutation of IQGAP1, or by treatment of cells with a phosphotidylinositol 3-kinase inhibitor. To determine the mechanism by which IQGAP1 overexpression affected hepatocellular carcinoma cells, we confirmed its interaction in these cells with mammalian target of rapamycin (mTOR), a serine/threonine kinase that integrates signals about nutrient and energy status with downstream effectors that influence cell division. In addition, we discovered a new interaction involving IQGAP1, mTOR and Akt, which is a downstream target of mTOR. Akt phosphorylation on Ser-473, which is catalyzed by mTOR and required for Akt activation, increased with increasing amounts of IQGAP1, and decreased with IQGAP1 mutation. We hypothesize that IQGAP1 is a scaffold that facilitates mTOR and Akt interaction.

HOCl Oxidation-modified CT26 Cell Vaccine Inhibits Colon Tumor Growth in a Mouse Model

Zhou, Rui,Huang, Wen-Jun,Ma, Cong,Zhou, Yan,Yao, Yu-Qin,Wang, Yu-Xi,Gou, Lan-Tu,Yi, Chen,Yang, Jin-Liang Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.8

Despite progress in elucidating mechanisms associated with colorectal cancer and improvement of treatment methods, it remains a frequent cause of death worldwide. New and more effective therapies are therefore urgently needed. Recent studies have shown that immunogenicity of whole ovarian tumor cells and subsequent T cell response were potentiated by oxidation modification with hypochlorous acid (HOCl) in vitro and ex vivo. These results prompted us to investigate the protective antitumor response with an HOCl treated CT26 colorectal cancer cell vaccine in an in vivo mouse model. Administration of HOCl modified vaccine triggered robust antitumor immunity to autologous tumor cells in mice and prolonged survival period significantly. In addition, increased necrosis and apoptosis were found in tumor tissue from the oxidation group. Interestingly, ELISPOT assays showed that specific T cell responses were not elicited in response to the immunizing cellular antigen, in contrast to raising sera antibody titer and antibody binding activity shown by ELISA assay and flow cytometry. Further evaluation of the mechanisms underlying HOCl modified vaccine mediated humoral immunity highlighted the role of antibody-dependent cell-mediated cytotoxicity. These results combined with previous studies suggest that HOCl oxidation modified whole cell vaccine has wide applicability as a cancer vaccine because it can target both T cell- and B cell-specific responses. It may thus represent a promising approach for the immunotherapy of colorectal cancer.

Correlations Between Serum IL33 and Tumor Development: a Meta-analysis

Chen, Xiang-Jun,Huang, Ying-De,Li, Nian,Chen, Min,Liu, Fang,Pu, Dan,Zhou, Tao-You Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.8

Background: Interleukin-33 (IL-33) has recently been implicated in tumor development. Methods: Data was obtained from PubMed, EMBASE, Clinical trial, Cochrane Library, Web of Science, CNKI and Wanfang databases. After quality assessment and data extraction, a meta-analysis was performed using Review Manager 5.2 software. Results: There were eight documents included in this meta-analysis. The results showed IL33 levels to be higher in tumor patients than that in health people, but no correlations tumor stage, metastasis and survival time of tumor patients were evident. Conclusion: IL33 may be useful as an alarm factor in tumor detection and prognosis.

ETV4 facilitates proliferation, migration, and invasion of liver cancer by mediating TGF-β signal transduction through activation of B3GNT3

Zhou Zhongcheng,Wu Bin,Chen Jing,Shen Yiyu,Wang Jing,Chen Xujian,Fei Faming,Li Liang 한국유전학회 2023 Genes & Genomics Vol.45 No.11

Background Metastasis of liver cancer (LC) is the main cause of its high mortality. ETV4 is a critical regulatory factor in promoting LC progression, but the mechanism that ETV4 impacts LC proliferation, migration, and invasion is poorly understood. Objective Investigation of the molecular mechanism of LC metastasis is conducive to developing effective drugs that prevent LC metastasis. Methods Expression of ETV4 and its target gene B3GNT3 in LC tissue was analyzed by bioinformatics, and the result was further verified in LC cells by qRT-PCR. In vitro cellular assays evaluated the impact of ETV4 on the proliferation, migration, and invasion of LC cells. Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter gene assay were conducted to analyze the interaction between B3GNT3 and ETV4. SB525334 suppressor was used to treat and access the activation of ETV4 on the TGF-β pathway. Results We discovered that ETV4 and B3GNT3 were evidently up-regulated in LC, and high expression of ETV4 was coupled to the increase of proliferation, migration, and invasion of LC cells and epithelial-mesenchymal transition ability. Besides, ETV4 could bind to the B3GNT3 promoter and activate its transcription. Knockdown of B3GNT3 could prominently suppress the effect of up-regulated ETV4 on LC cells. Meanwhile, ETV4 could activate the TGF-β signaling pathway via B3GNT3, while SB525334 treatment notably repressed the functions of ETV4. Conclusion ETV4 emerges as a driven oncogene in LC, and the ETV4/B3GNT3-TGF-β pathway promotes proliferation, migration, invasion, and epithelial-mesenchymal transition progress of LC. Inhibition of the pathway may provide an underlying method for the prevention and treatment of LC metastasis.

Coupling method of magnetic memory and eddy current nondestructive testing for retired crankshafts

Chen Ni,Lin Hua,Xiaokai Wang,Zhou Wang,Xunpeng Qin,Zhou Fang 대한기계학회 2016 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.30 No.7

To verify the validity of the Coupling method of magnetic memory and eddy current (CMMEC) testing for crankshafts, we use this technique to test a 12-cylinder V-design diesel crankshaft. First, the stress distribution in the crankshaft was obtained under 12 working conditions using a Finite element (FE) model that complied with the commercial FE code ABAQUS. Second, Magnetic memory testing (MMT) and Eddy current testing (ECT) were adopted to detect the regions of stress concentration in the crankshaft and the specific location of cracks based on simulation results. Lastly, magnetic particle testing was conducted to detect and display the corresponding crack to verify the CMMEC testing results. The MMT and ECT results can provide basis and guidance for the remanufacture and life evaluation of retired crankshafts.

Analysis of Small Fragment Deletions of the APC gene in Chinese Patients with Familial Adenomatous Polyposis, a Precancerous Condition

Chen, Qing-Wei,Zhang, Xiao-Mei,Zhou, Jian-Nong,Zhou, Xin,Ma, Guo-Jian,Zhu, Ming,Zhang, Yuan-Ying,Yu, Jun,Feng, Ji-Feng,Chen, Sen-Qing Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.12

Background: : Familial adenomatous polyposis (FAP) is an autosomal dominant inherited disease mainly caused by mutations of the adenomatous polyposis coli (APC) gene with almost complete penetrance. These colorectal polyps are precancerous lesions that will inevitable develop into colorectal cancer at the median age of 40-year old if total proctocolectomy is not performed. So identification of APC germline mutations has great implications for genetic counseling and management of FAP patients. In this study, we screened APC germline mutations in Chinese FAP patients, in order to find novel mutations and the APC gene germline mutation characteristics of Chinese FAP patients. Materials and Methods: The FAP patients were diagnosed by clinical manifestations, family histories, endoscope and biopsy. Then patients peripheral blood samples were collected, afterwards, genomic DNA was extracted. The mutation analysis of the APC gene was conducted by direct polymerase chain reaction (PCR) sequencing for micromutations and multiplex ligation-dependent probe amplification (MLPA) for large duplications and/or deletions. Results: We found 6 micromutations out of 14 FAP pedigrees, while there were no large duplications and/or deletions found. These germline mutations are c.5432C>T(p. Ser1811Leu), two c.3926_3930delAAAAG (p.Glu1309AspfsX4), c.3921_3924delAAAA (p.Ile1307MetfsX13), c3184_3187delCAAA(p.Gln1061AspfsX59) and c4127_4126delAT (p.Tyr1376LysfsX9), respectively, and all deletion mutations resulted in a premature stop codon. At the same time, we found c.3921_3924delAAAA and two c.3926_3930delAAAAG are located in AAAAG short tandem repeats, c3184_3187delCAAA is located in the CAAA interrupted direct repeats, and c4127_4128 del AT is located in the 5'-CCTGAACA-3', 3'-ACAAGTCC-5 palindromes (inverted repeats) of the APC gene. Furthermore, deletion mutations are mostly located at condon 1309. Conclusions: Though there were no novel mutations found as the pathogenic gene of FAP in this study, we found nucleotide sequence containing short tandem repeats and palindromes (inverted repeats), especially the 5 bp base deletion at codon 1309, are mutations in high incidence area in APC gene,.

Significant Association of Alpha-Methylacyl-CoA Racemase Gene Polymorphisms with Susceptibility to Prostate Cancer: a Meta-Analysis

Chen, Nan,Wang, Jia-Rong,Huang, Lin,Yang, Yang,Jiang, Ya-Mei,Guo, Xiao-Jiang,He, Ya-Zhou,Zhou, Yan-Hong Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.5

Background: Alpha-methylacyl-CoA racemase(AMACR) is thought to play key roles in diagnosis and prognosis of prostate cancer. However, studies of associations between AMACR gene polymorphisms and prostate cancer risk reported inconsistent results. Therefore, we conducted the present meta-analysis to clarify the link between AMACR gene polymorphisms and prostate cancer risk. Materials and Methods: A literature search was performed in PubMed, Embase, China National Knowledge Infrastructure (CNKI), Wanfang and Weipu databases. Odds ratios (ORs) and 95% confidence intervals (95%CIs) were calculated to assess the strength of any association between AMACR polymorphisms and prostate cancer risk. Subgroup analyses by ethnicity, source of controls, quality control and sample size were also conducted. Results: Five studies covering 3,313 cases and 3,676 controls on five polymorphisms (D175G, M9V, S201L, K277E and Q239H) were included in this meta-analysis. Significant associations were detected between prostate cancer and D175G (dominant model: OR=0.89, 95%CI=0.80-0.99, P=0.04) and M9V (dominant model: OR=0.87, 95%CI=0.78-0.97, P=0.01) polymorphisms as well as that in subgroup analyses. We also observed significant decreased prostate cancer risk in the dominant model (OR=0.90, 95%CI=0.81-0.99, P=0.04) for the S201L polymorphism. However, K277E and Q239H polymorphisms did not appear to be related to prostate cancer risk. Conclusions: The current meta-analysis indicated that D175G and M9V polymorphisms of the AMACR gene are related to prostate cancer. The S201L polymorphism might also be linked with prostate cancer risk to some extent. However, no association was observed between K277E or Q239H polymorphisms and susceptibility to prostate cancer.