Decomposition-based Gradient Estimation Algorithms for Multivariable Equation-error Systems

Xian Lu,Feng Ding,Ahmed Alsaedi,Tasawar Hayat 제어·로봇·시스템학회 2019 International Journal of Control, Automation, and Vol.17 No.8

This paper concerns the parameter identification methods of multivariable equation-error systems. By means of the decomposition technique, the multivariable identification model is transformed into two subidentification models and a decomposition-based stochastic gradient (D-SG) algorithm is presented for estimating the parameters of these two submodels. In order to further improve the convergence rate and the parameter estimation accuracy, we expand the innovation vectors to the innovation matrices and develop a decomposition-based multi-innovation stochastic gradient (D-MISG) algorithm. The simulation results confirm that the D-MISG algorithm can provide more accurate parameter estimates than the D-SG algorithm.

Chromatin-remodeling Factor INI1/hSNF5/BAF47 Is Involved in Activation of the Colony Stimulating Factor 1 Promoter

Xianlu Zeng,Xuefang Pan,Zhaoxia Song,Lei Zhai,Xiaoyun Li 한국분자세포생물학회 2005 Molecules and cells Vol.20 No.2

INI1/hSNF5/BAF47 is a core component of the hSWI/ SNF ATP-dependent chromatin remodeling complex,and it has been implicated in regulating gene expression, cell division and tumorigenesis. We investigated whether INI1/hSNF5/BAF47 functions in activation of the colony stimulating factor 1 (CSF1) promoter in HeLa cells. Overexpression of INI1/hSNF5/BAF47 promoted CSF1 transcription, and siRNA targeting INI1/hSNF5/ BAF47 (siINI1) strongly inhibited the activity of the CSF1 promoter. We demonstrated that all conserved domains of INI1/hSNF5/BAF47 are needed for CSF1 transcription. ChIP experiment showed that INI1/ hSNF5/BAF47 is recruited to the region of the CSF1 promoter. Taken together, these results indicate that INI1/hSNF5/BAF47 is involved in activation of the CSF1 promoter

SERPINE1 as an Independent Prognostic Marker and Therapeutic Target for Nicotine-Related Oral Carcinoma

Xiaopeng Guo,Xianlu Zhuo,Zhen Sun,Huarong Chen,Junjun Ling,Houyu Zhao,Aoshuang Chang 대한이비인후과학회 2023 Clinical and Experimental Otorhinolaryngology Vol.16 No.1

Objectives. Nicotine is an ingredient of tobacco, and exposure to nicotine increases the risks of various cancers, includingoral cancer. Previous studies have focused on the addictive properties of nicotine, but its carcinogenic mechanism hasrarely been studied. We aimed to explore the key genes in the process through which nicotine promotes the occur-rence and development of oral cancer via data mining and experimental verification. Methods. This study involved three parts. First, key genes related to nicotine-related oral cancer were screened throughdata mining; second, the expression and clinical significance of a key gene in oral cancer tissues were verified by bio-informatics. Finally, the expression and clinical significance of the key gene in oral cancer were histologically investi-gated, and the effects of its expression on cell proliferation, invasion, and drug resistance were cytologically assessed. Results. SERPINE1 was identified as the key gene, which was upregulated in nicotine-treated oral cells and may be an in-dependent prognostic factor for oral cancer. SERPINE1 was enriched in various pathways, such as the tumor necro-sis factor and apelin pathways, and was related to the infiltration of macrophages, CD4+T cells, and CD8+T cells. Overexpression of SERPINE1 was associated with N staging and may be involved in hypoxia, angiogenesis, and me-tastasis. Knockdown of SERPINE1 in oral cancer cells resulted in weakened cell proliferation and invasion abilityand increased sensitivity to bleomycin and docetaxel. Conclusion. This study revealed SERPINE1 as a key gene for nicotine-related oral cancer, indicating that SERPINE1 maybe a novel prognostic indicator and therapeutic target for oral carcinoma.

Identification of Nucleolin as a Lipid-Raft-Dependent Beta1-Integrin-Interacting Protein in A375 Cell Migration

Jiajia Bi,Xianlu Zeng,Ruifei Wang,Yue Zhang,Xiaoqing Han,Khamal Kwesi Ampah,Wenguang Liu 한국분자세포생물학회 2013 Molecules and cells Vol.36 No.6

Lipid rafts are related to cell surface receptor function. Integrin is a major surface receptor protein in cell adhesion and migration on the extracellular matrix (ECM). Here, we showed that lipid rafts played a critical role in human melanoma A375 cell spreading and migration on fibronectin; an important component of the ECM that interacts with 1 integrin. We found that the disruption of lipid rafts did not markedly inhibit the expression and activation of 1 integrin. By coimmunoprecipitation and mass spectrometry, we investigated the influence of lipid rafts on the 1 integrin complex and identified nucleolin as a potential lipid-raft-dependent 1-integrin-interacting protein. Upon confirmation of the interaction between 1 integrin and nucleolin, further studies revealed that nucleolin colocalized with 1 integrin in lipid rafts and raft disruption interrupted their association. In addition, knockdown of nucle-olin markedly attenuated A375 cell spreading and migration on fibronectin. Taken together, we demonstrated that nucleolin is a critical lipid-raft-dependent 1-integrin-inte-racting protein in A375 cell spreading and migration on fibronectin.

β-Actin regulates interleukin 6-induced p21 transcription by interacting with the Rpb5 and Rpb7 subunits of RNA polymerase II

Xiujuan Tian,Wenjing Qi,Hongyu Chen,Xianlu Zeng,Liping Han,Donghui Mi 한국통합생물학회 2016 Animal cells and systems Vol.20 No.5

In pre-initiation complexes, RNA helicase A interacts with β-actin and acts as a bridging factor linking nuclear actin with RNA polymerase II (Pol II). In addition, β-actin participates in Pol IIdependent transcription elongation by interacting with the positive transcription elongation factor Cdk9. However, many relationships between β-actin and Pol II remain to be identified. In an interleukin 6 (IL-6)-induced p21 expression model, we demonstrated that β-actin knockdown reduced p21 expression. Immunofluorescence analysis showed that the colocalization of β-actin and Pol II increased significantly in cells treated with IL-6. It is known that the Rpb5, Rpb6 and Rpb7 subunits are located at the surface of the enzyme. We next constructed recombinant pcDNA-HA-Rpb5, pcDNA-HA-Rpb6 and pcDNA-HA-Rpb7 plasmids and expressed the three polymerase II subunits in HepG2 cells. We found that β-actin could be immunoprecipitated with HA-Rpb5 and HA-Rpb7. A Glutathione-S-transferase pull-down assay revealed that β-actin was associated with Rpb5 and Rpb7 in vitro. Furthermore, overexpression of Rpb5 and Rpb7 in cells reduced p21 expression significantly, suggesting that Rpb5 and Rpb7 competitively interact with β-actin. This study shows that β-actin associates with Pol II subunits through direct proteinprotein interactions and provides fundamental insight into Pol II transcriptional regulation.

Leukotriene B4 Regulates Proliferation and Differentiation of Cultured Rat Myoblasts via the BLT1 Pathway

Ru Sun,Xueqing Ba,Lingling Cui,Yan Xue,Xianlu Zeng 한국분자세포생물학회 2009 Molecules and cells Vol.27 No.4

Skeletal muscle regeneration is a highly orchestrated process initiated by activation of adult muscle satellite cells. Upon muscle injury, the inflammatory process is always accompanied by muscle regeneration. Leukotriene B4 is one of the essential inflammatory mediators. We isolated and cultured primary satellite cells. RT-PCR showed that myoblasts expressed mRNA for LTB4 receptors BLT1 and BLT2, and LTB4 promoted myoblast proliferation and fusion. Quantitative real-time PCR and immunoblotting showed that LTB4 treatment expedited the expression process of differentiation markers MyoD and M-cadherin. U-75302, a specific BLT1 inhibitor, but not LY2552833, a specific BLT2 inhibitor, blocked proliferation and differentiation of myoblasts induced by LTB4, which implies the involvement of the BLT1 pathway. Overall, the data suggest that LTB4 contributes to muscle regeneration by accelerating proliferation and differentiation of satellite cells.

P-Selectin-mediated Acute Inflammation Can Be Blocked by Chemically Modified Heparin, RO-Heparin

Yanguang Gao,Na Li,Rui Fei,Zhihong Chen,Sheng Zheng,Xianlu Zeng 한국분자세포생물학회 2005 Molecules and cells Vol.19 No.3

Selectins are carbohydrate-binding cell adhesion molecules that play a major role in the initiation of inflammatory responses. Heparin can bind to P-selectin, and its anti-inflammatory property is mainly due to inhibition of P-selectin. However, the strong anticoagulant activity of heparin limits its clinical use. We prepared periodate-oxidized, borohydride-reduced heparin (ROheparin) by chemical modification and tested its anticoagulant and anti-inflammatory activities. Activated partial thromboplastin time (aPTT) assays showed that, compared with heparin, RO-heparin had greatly reduced anticoagulant activity. Intravenous administration of this compound led to reduction in the peritonealinfiltration of neutrophils in a mouse acute inflammation model. In vitro cell adhesion experiments demonstrated that the effect of RO-heparin on inflammatory responses was mainly due to inhibiting the interaction of P-selectin with its ligands. These results indicate that RO-heparin may be a safer treatment for inflammation than heparin, especially when selectin is targeted.

MicroRNA 449c Mediates the Generation of Monocytic Myeloid-Derived Suppressor Cells by Targeting STAT6

Han, Xiaoqing,Luan, Tao,Sun, Yingying,Yan, Wenyi,Wang, Dake,Zeng, Xianlu Korean Society for Molecular and Cellular Biology 2020 Molecules and cells Vol.43 No.9

Myeloid-derived suppressor cells (MDSCs) promote tumour progression by contributing to angiogenesis, immunosuppression, and immunotherapy resistance. Although recent studies have shown that microRNAs (miRNAs) can promote the expansion of MDSCs in the tumour environment, the mechanisms involved in this process are largely unknown. Here, we report that microRNA 449c (miR-449c) expression was upregulated in myeloid progenitor cells upon activation of C-X-C motif chemokine receptor 2 (CXCR2) under tumour conditions. MiR-449c upregulation increased the generation of monocytic MDSCs (mo-MDSCs). The increased expression of miR-449c could target STAT6 mRNA in myeloid progenitor cells to shift the differentiation balance of myeloid progenitor cells and lead to an enhancement of the mo-MDSCs population in the tumour environment. Thus, our results demonstrate that the miR-449c/STAT6 axis is involved in the expansion of mo-MDSCs from myeloid progenitor cells upon activation of CXCR2, and thus, inhibition of miR-449c/STAT6 signalling may help to attenuate tumour progression.