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author:("Xu, xinghua")
1.  Inhibition of the angiogenesis and growth of Aloin in human colorectal cancer in vitro and in vivo 
Background
Angiogenesis has been an attractive target for drug therapy. Aloin (AL), an natural compound derived from Aloe barbadensis Miller leaves, has been shown to possess anti-cancer potential activities. However, its roles in tumor angiogenesis and the involved molecular mechanism are unknown.
Method
To evaluate the antiangiogenic and anticancer activities of AL, endothelial cell scratch, modified Boyden chamber inserts and tube formation assays were done in HUVECs, and MTT and Live-Dead assays were used to determine the proliferation inhibition and apoptosis induction of colorectal cancer cells in vitro. The inhibition effects of AL were further confirmed by a mouse xenograft model in vivo. The expression levels of STAT3 signaling pathway and that mediated-target genes were measured in HUVECs and SW620 cells by Western blots.
Results
Here, we demonstrated that AL significantly inhibited HUVECs proliferation, migration and tube formation in vitro. Western blotting showed that AL suppressed activation of VEGF receptor (VEGFR) 2 and STAT3 phosphorylation in endothelial cells. In addition, the constitutively activated STAT3 protein, and the expression of STAT3-regulated antiapoptotic (Bcl-xL), proliferative (c-Myc), and angiogenic (VEGF) proteins were also down-regulated in response to AL in human SW620 cancer cells. Consistent with the above findings, AL inhibited tumor cell viability and induced cell apoptosis in vitro, and substantially reduced tumor volumes and weight in vivo mouse xenografts, without obviously toxicity.
Conclusion
Our studies provided the first evidence that AL may inhibit tumor angiogenesis and growth via blocking STAT3 activation, with the potential of a drug candidate for cancer therapy.
doi:10.1186/1475-2867-13-69
PMCID: PMC3722112  PMID: 23848964
Aloin; Angiogenesis; Tumor growth; Colorectal cancer; STAT3
2.  Active autophagy in the tumor microenvironment: A novel mechanism for cancer metastasis 
Oncology Letters  2012;5(2):411-416.
Autophagy is a lysosomal degradation process which is key for the regulation of the turnover of long-lived or damaged proteins and organelles and which promotes cell survival during nutrient deprivation or other microenvironmental stresses. Current evidence supports the hypothesis that autophagy suppresses tumorigenesis, particularly during the early stages of tumor initiation. However, in established tumors, autophagy promotes survival under stressful conditions during cancer progression and in response to chemotherapy; however, the mechanism by which autophagy influences cancer metastasis remains unknown. In this review, we discuss the capacity of an abnormal tumor environment to induce autophagy and consider how this relates to tumor metastasis and the attractive prospect of manipulating autophagic signaling pathways as potential targets for the treatment of cancer metastasis.
doi:10.3892/ol.2012.1015
PMCID: PMC3573143  PMID: 23420500
autophagy; microenvironment; metastasis; pathway; cancer
3.  Complete Genome Sequence of Bordetella pertussis CS, a Chinese Pertussis Vaccine Strain ▿  
Journal of Bacteriology  2011;193(15):4017-4018.
Bordetella pertussis is the causative agent of pertussis. Here, we report the genome sequence of Bordetella pertussis strain CS, isolated from an infant patient in Beijing and widely used as a vaccine strain for production of an acellular pertussis vaccine in China.
doi:10.1128/JB.05184-11
PMCID: PMC3147532  PMID: 21622744
4.  Effect of Vaccination on Bordetella pertussis Strains, China 
Emerging Infectious Diseases  2010;16(11):1695-1701.
Strains in China may differ from those in countries that have long histories of high vaccination coverage.
Whole-cell pertussis vaccine was introduced in China in the early 1960s. We used standard typing methods to compare 96 Bordetella pertussis isolates collected before and after introduction of vaccination, during 1953–2005. The following vaccine-type alleles of the pertussis toxin (ptx) gene were characteristic for all prevaccination strains: ptxA2, ptxA3, and ptxA4. The shift to ptxA1 occurred since 1963. All isolates collected since 1983 contained ptxA1. Pertactin (prn) allele 1, prn1, was predominant, although prn2 and prn3 have been detected since 2000. Serotypes fimbriae (Fim) 2 and Fim2,3 were found in all isolates collected before 1986. During 1997–2005, Fim3 became prevalent. Although changes in electrophoresis profiles over time were observed, the predominant profiles during 1997–2005 resembled those during the prevaccine era and those found in Europe before the 1990s. B. pertussis strains in China may differ from those in countries that have a long history of high vaccine coverage.
doi:10.3201/eid1611.100401
PMCID: PMC3294513  PMID: 21029526
China; Bordetella pertussis; whooping cough; pertussis; incidence; vaccination; genotyping; PFGE; bacteria; research
5.  Production and characterization of recombinant pertactin, fimbriae 2 and fimbriae 3 from Bordetella pertussis 
BMC Microbiology  2009;9:274.
Background
Bordetella pertussis is a causative agent of pertussis or whooping cough in humans. Pertactin (Prn), fimbriae 2 (Fim2) and fimbriae 3 (Fim3) of B. pertussis are important virulence factors and immunogens which have been included in some acellular pertussis vaccines. In this present study, we cloned, expressed and purified Prn, Fim2 and Fim3, respectively. The immunogenicity and protective efficacy of the three recombinant proteins (rPrn, rFim2 and rFim3) were investigated in mouse model.
Results
Three recombinant proteins with amount of 12 to 25 mg/L were produced. Compared to the control mice only immunized with adjuvant, serum IgG antibody responses were significantly induced in the mice immunized with rPrn, rFim2 or rFim3 (P < 0.001 for all three proteins). Furthermore, T cell responses characteristic of increased production of IL-2 and TNF-α (only for rPrn) were elicited in the mice immunized with the three proteins (P < 0.05 for all three proteins). Immunization with rPrn, but not with rFim2 or rFim3, significantly enhanced clearance of bacteria in the lungs of mice after intranasal challenge with B. pertussis (P < 0.05). When tested in a lethal intracerebral infection model, certain protection was observed in mice immunized with rPrn.
Conclusions
We have developed an efficient method to produce large amounts of rPrn, rFim2, and rFim3 from B. pertussis. The three recombinant proteins induced both humoral and cellular immune responses in mice. Immunization with rPrn also conferred protection against pertussis in mouse infection models. Our results indicated that the recombinant proteins still retain their immunological properties and highlighted the potential of the recombinant proteins for the future development of the B. pertussis vaccines.
doi:10.1186/1471-2180-9-274
PMCID: PMC2807877  PMID: 20040101
6.  The Basic Science of Tendinopathy 
Tendinopathy is a common clinical problem with athletes and in many occupational settings. Tendinopathy can occur in any tendon, often near its insertion or enthesis where there is an area of stress concentration, and is directly related to the volume of repetitive load to which the tendon is exposed. Recent studies indicate tendinopathy is more likely to occur in situations that increase the “dose” of load to the tendon enthesis – including increased activity, weight, advancing age, and genetic factors. The cells in tendinopathic tendon are rounder, more numerous, and show evidence of oxidative damage and more apoptosis. These cells also produce a matrix that is thicker and weaker with more water, more immature and cartilage-like matrix proteins, and less organization. There is now evidence of a population of regenerating stem cells within tendon. These studies suggest prevention of tendinopathy should be directed at reducing the volume of repetitive loads to below that which induces oxidative-induced apoptosis and cartilage-like genes. The management strategies might involve agents or cells that induce tendon stem cell proliferation, repair and restoration of matrix integrity.
doi:10.1007/s11999-008-0286-4
PMCID: PMC2505234  PMID: 18478310

Results 1-6 (6)