Yong Xu

Baylor College of Medicine

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Ranlu Liu

Second Hospital of Tianjin Medical University

Quynh Nguyen

Oxford University Clinical Research Unit

Jingjing Pan

Xi'an Chest Hospital

Linjun Tang

Wuhu Fourth People Hospital

Mei Zhang

Chinese Academy of Medical Sciences & Peking Union Medical College

Chengying Hong

Southern University of Science and Technology

Cody Zurhellen

Caleb A. Wood

Baylor College of Medicine

Zhen-quan Jiao

Chinese Center For Disease Control and Prevention

Peter J. Kim

Baylor College of Medicine

Cooperative Institutions

Baylor College of Medicine

Nanjing Medical University

Huazhong University of Science and Technology

Anhui Medical University

Sichuan University

Chinese Academy of Medical Sciences & Peking Union Medical College

The University of Texas Health Science Center at Houston

Tianjin Medical University

Soochow University

First Affiliated Hospital of Anhui Medical University

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[The effects of acrylonitrile on cell apoptosis, proliferation and related genes expression of rat normal and tumor glial cells].

Zhen-quan Jiao Yunchang Guo Yong Xu

Objective To study the effect of acrylonitrile(CAN)to cell growth,apoptosis,proliferation and related gene expression of rat normal glial ceUs(DI TNCI)and tumor glial cells(C6).Methods The concentration of CAN on DI TNCI and C6 were 25,50 and 75μg/mL For cell growth,prolifcration and apoptosis assay,the treated time was 24 hours.for microarray assay,the treated time wa84 and 24 houm.Results After treatment of DI TNCl cell with 25,50 and 75μ/ml CAN,the DNA synthesis index were decreased 93.1%.81.3%and 74.9%as compared to control respectively,the apoptosis index Was increased 118%.122%and 143%as compared to controls respectively.The DNA syntllesis and apoptosis indexes of C6 cell showed no change after treatment with CAN.The cell cycle and apoptosis pathway related genes,such as cyclin and p53,also showed changes after treatment with AC N.Conclusion CAN inhibited the cell proliferation of DI TNCl.induced the apoptosis of DI TNCl and had no effect on cell proliferation and apoptosis of C6 cells,and the related regulation gene expression changes further confirmed the results. Key words: Acrylonitrile; Cell proliferation; Apoptosis; Bats; Neurog]ia

Proliferation index

10.3321/j.issn:0253-9624.2008.06.008

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Citations (2)

[Cadherin switching induced by P120-catenin can promote the migration and invasion of oral squamous cell cancer cells].

PubMed (2017)

Zhong Chen Mei Zhang Yong Xu

The main goal is to investigate the role of P120-catenin (P120ctn) in cadherin switching, as well as migration and invasion, of oral squamous cell cancer (OSCC) cells.The plasmid pGFP-V-RS-P120ctn shRNA was used to transfect TSCCA cells and significantly reduce the expression of P120ctn in these cells. Real-time fluorescent quantitative polymerase chain reaction and Western blot were conducted to determine the mRNA and protein expression levels of P120ctn, E-cadherin (E-cad), and N-cadherin (N-cad). By contrast, the Transwell cell invasion and cell migration assay was used to determine the invasion and migration capacities before and after the transfection.After the plasmid pGFP-V-RS-P120ctn shRNA was transfected into the TSCCA cells, we found that as the P120ctn expression significantly decreased, E-cad mRNA and protein expression decreased significantly. Moreover, N-cad mRNA and protein expression increased significantly (P<0.05). Lastly, the cell migration and invasion capacities were augmented significantly (P<0.05).In OSCC cells, P120ctn may be involved in cadherin switching and promote metastasis and invasion.目的探索P120-连环蛋白（P120ctn）在口腔鳞状细胞癌（OSCC）细胞钙黏蛋白转换中的作用及其对肿瘤细胞迁移和侵袭的影响。方法采用质粒pGFP-V-RS-P120ctn shRNA转染OSCC细胞株TSCCA，采用实时荧光定量聚合酶链反应、Western blot检测细胞中P120ctn、E-钙黏蛋白（E-cad）和N-钙黏蛋白（N-cad）的mRNA和蛋白表达的变化，通过Transwell细胞侵袭及细胞迁移实验检测转染前后细胞迁移和侵袭能力的变化。结果质粒pGFP-V-RS-P120ctn shRNA转染TSCCA细胞后，P120ctn表达明显降低，E-cad的mRNA和蛋白表达水平也明显降低，而N-cad的mRNA和蛋白表达水平明显提高，细胞迁移和侵袭能力也明显提高，差异均有统计学意义（P<0.05）。结论在OSCC中P120ctn可能通过介导钙黏蛋白转换来调节肿瘤的浸润和转移过程。.

10.7518/hxkq.2017.02.014

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Downregulation of Nucleostemin Causes G1 Cell Cycle Arrest via a p53-Independent Pathway in Prostate Cancer PC-3 Cells

Urologia Internationalis (2010)

Ranlu Liu Zhihong Zhang Yong Xu

Aims: To screen the genes and possible signal transduction pathways with which nucleostemin (NS) interacts and explore the mechanism of NS in prostate cancer. Methods: NS-specific short-hairpin RNA expression plasmid was used to downregulate the NS level in PC-3 cells and the changes of cell cycle were studied. After that, oligonucleotide DNA microarray was used to screen the genome changes in PC-3 cells and quantitative real-time PCR was used to further confirm the differentially expressed genes. Results: Detection of cell cycle showed a decrease of S stage and an increase of G1 stage after downregulation of NS. 219 differentially expressed genes were found and these genes were involved in cell cycle, cell proliferation, signal transduction, cell apoptosis and cell differentiation, and so on. Genes related to cell cycle were discussed emphatically. INK4 family genes (P15, P16, P18) were upregulated while cyclin D1 HDAC1 were downregulated. These genes were tightly related to CDK4/6-cyclin D and pRb-E2F1 complexes. Conclusion: NS is an important G1/S checkpoint regulator and it could regulate cell cycles via a p53-independent pathway in prostate cancer.

Cyclin B1

Cyclin E1

Retinoblastoma protein

10.1159/000315968

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Expression of nucleostemin in prostate cancer and its effect on the proliferation of PC-3 cells

Chinese Medical Journal (2008)

Ranlu Liu Zhihong Zhang Weiming Zhao Meng Wang Shiyong Qi

Background Nucleostemin is essential for the proliferation and survival of stem and cancer cells, but it is unknown whether this newly identified molecule is involved in prostate cancer pathogenesis. Methods Total RNA and protein were extracted from prostate cancer tissues and PC-3, LNCap and DU145 cell lines. The nucleostemin mRNA and protein expression were measured by RT-PCR and Western blot. Immunohistochemistry was also used to detect the nucleostemin protein expression in prostate cancer tissues and PC-3 cells. A nucleostemin specific, short hairpin RNA, expression plasmid was used to transfect PC-3 cells. The changes of nucleostemin gene were detected and the proliferative capacity of the cells was determined. Results Nucleostemin was highly expressed in prostate cancer tissues and cell lines. Nucleostemin expression level in the silencer group PC-3 cells remarkably reduced. The proliferation rate of silencer group PC-3 cells decreased and the percentage of G1 stage cells increased. The neoplasm forming capacity in nude mice of the silencer group PC-3 cells decreased significantly. Conclusions Nucleostemin is highly expressed in prostate cancer tissues and cell lines. The proliferative capacity of PC-3 cells is remarkably reduced after silencing nucleostemin gene expression.

DU145

10.1097/00029330-200802020-00004

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Adipose-derived stem cell exosomes ameliorate traumatic brain injury through the NLRP3 signaling pathway

Neuroreport (2023)

Linjun Tang Yong Xu Handong Wang Jingjing Pan

The exosomes of mesenchymal stem cells have immunoregulatory properties and can effectively mitigate secondary neuroinflammation due to traumatic brain injury (TBI). In this study, we found that adipose-derived stem cell exosomes (ADSCs-Exo) could reduce the inflammatory response after traumatic brain injury by reducing NLRP3 inflammasome secretion by microglial. ADSCs-Exo were monitored by Western blot and electron microscopy. An in-vitro lipopolysaccharide (LPS)-caused primary microglia model and a TBI rat model were constructed. Functional recovery was examined using the modified neurological severity score and foot fault tests. Inflammasome inactivation in LPS-stimulated microglial, ADSCs-Exo can reduce the secretion of interleukin (IL)-1β, IL-6 and tumor necrosis factor α. Compared with PBS-processed controls, the sensorimotor functional recovery was significantly improved by exosome treatment after injury at 14–35 days. Additionally, NLRP3 inflammasome was stimulated within 24 h after TBI. ADSCs-Exo application led to remarkable down-expression of NLRP3 and caspase-1. ADSCs-Exo can ameliorate LPS-induced inflammatory activation by reducing microglial pro-inflammatory cytokines. Moreover, the neuroprotective effect of ADSCs-Exo may be partially attributed to the inhibition thereof on the formation of NLRP3-mediated inflammasome. Such findings imply a potential function of ADSCs-Exo in treating TBI.

Exosome

Microvesicle

10.1097/wnr.0000000000001941

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Advances in research on relationship between Toll-like receptor 4 and sepsis

Zhongguo shengwuzhipinxue zazhi (2012)

Yong Xu

Severe sepsis and sepsis shock are the major causes of deaths at present.Toll-like receptor 4(TLR4)is the receptor of lipopolysaccharide in cell walls of gram-negative bacteria.The genetic polymorphisms of TLR4 and its signal pathway play important roles in ongoing of sepsis.Most of the treatments against single inflammatory cytokine are declared fail.Because of the important role of TLR4,the targeting treatments against TLR4 and signal pathway are hopeful.This paper reviews the relationship of genetic polymorphisms of TLR4 and its signal pathway to the susceptibility and regulator of sepsis.

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Effect of parthenolide on proliferation and apoptosis in gastric cancer cell line SGC7901

Journal of Digestive Diseases (2009)

Li Jie ZHAO Yong Xu Yan Li

OBJECTIVE: To investigate the effect of parthenolide (PAR) on proliferation and apoptosis in gastric cancer cell line SGC7901. METHODS: Human gastric cancer cell line SGC7901 cells were incubated with various concentration of PAR. After various periods of incubation, the proliferation of SGC7901 cells was assessed by 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide methyl thiazolyl tetrazolium (MTT) assay. Apoptosis was measured by the annexin V‐fluorescein isothiocyanate fluoresceine isothiocyanate (FITC)/propidium iodide (PI) double labeled staining method and the morphology of the cell was observed under a fluorescent microscope. Mitochondrial potential was measured by flow cytometry after Rhodamine 123 staining. The expressions of cytochrome C and the Bcl‐2 family of proteins, including Bcl‐2, Bax, Bid and tBid were measured by Western blot. Caspase 3 and 8 activities were measured by enzyme‐linked immunosorbent assay. RESULTS: Treatment with PAR induced apoptosis as confirmed by annexin V‐FITC/PI assay. PAR‐induced apoptosis was associated with intracellular events including the decline of mitochondrial potential, increased release of cytochrome C from the mitochondria, decreased expression of Bcl‐2, increased expression of Bax, Bid and tBid and activation of caspase 3 and 8. CONCLUSION: These results suggest that possibly via activation of the mitochondrial pathway, PAR causes mitochondrial damage leading to the release of cytochrome C and by regulating the expression of the Bcl‐2 family of proteins and activating caspases which leads to results in apoptotic cell death in SGC7901 cells. Our results might be helpful in formulating new therapeutic approaches using Chinese herbal medicine.

Propidium iodide

Rhodamine 123

10.1111/j.1751-2980.2009.00382.x

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TMEM106B coding variant is protective and deletion detrimental in a mouse model of tauopathy

Acta Neuropathologica (2024)

George A. Edwards Caleb A. Wood Yang He Quynh Nguyen Peter J. Kim

Tauopathy

Cognitive Decline

10.1007/s00401-024-02701-5

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