Li Xue

Xi'an Jiaotong University, Ch’ang-an, Shaanxi, China

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Publications (8)23.21 Total impact

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    ABSTRACT: Background/Aims: Notch signaling pathway regulates cancer cell growth. RBPJ is a key transcription factor downstream of Notch receptor activation, whereas the role of RBPJ in carcinogenesis of prostate cancer is ill-defined. Methods: Here, we evaluated the effects of RBPJ inhibition on the growth of prostate cancer cells. We knocked down RBPJ in prostate cancer cells by a short hairpin interfering RNA (shRNA). We measured cell growth by an MTT assay. We analyzed the levels of cell-cycle-associated proteins by Western blot. Results: We found that shRNA for RBPJ efficiently inhibited RBPJ expression in prostate cancer cells, resulting in a significant decrease in the cell growth. Further, RBPJ-mediated cell-growth inhibition appeared to be resulting from alteration of cell-cycle inhibitors p21 and p27, cell-cycle activators CDK2, CDK4 and CyclinD1, and apoptosis-suppressor Bcl-2. Conclusion: Our data suggest that shRNA intervention of RBPJ expression could be a promising therapeutic approach for treating human prostate cancer.
    Cellular Physiology and Biochemistry 07/2015; 36(5):1982-1990. DOI:10.1159/000430166 · 2.88 Impact Factor
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    ABSTRACT: The p53 gene and MDM2 gene play critical roles in cell cycle arrest and apoptosis together. Here, we evaluated the associations of prostate cancer risk and survival with the joint effects of mdm2 and p53 polymorphisms. Totally 1,193 cases and 1,310 age frequency-matched controls were included in the study. Prostate cancer patients were followed to determine the intervals of overall survival and disease-free survival. The Pro72Arg Pro allele (homozygous and heterozygous) were significantly associated with prostate cancer risk with an odds ratio (OR) of 0.77 [95% confidence interval(CI), 0.64-0.93]. SNP309 T alleles were associated with a significantly decreased prostate cancer risk among Pro72Arg Pro alleles carriers (OR=0.79, 95% CI, 0.64-0.98). In addition, comparedwith the Pro72Arg Pro alleles and SNP309 G homozygous, patients carrying both SNP309 T alleles and Pro72Arg Arg homozygous had more favorable disease-free survival (hazard ratio [HR] = 0.59, 95% CI, 0.38-0.93). Our results indicated that SNP309 and Pro72Arg polymorphisms may jointly contributeto the etiology and prognosis of prostate cancer.
    Oncotarget 05/2015; DOI:10.18632/oncotarget.3923 · 6.36 Impact Factor
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    ABSTRACT: Proteins of the protein tyrosine phosphatase (PTP) family are known to be signaling molecules that regulate a variety of cellular processes including cell growth, differentiation, and apoptosis. PTPN13 (also known as FAP1, PTPL1, PTPLE, PTPBAS, and PTP1E), a putative tumor suppressor, is frequently inactivated in lung carcinoma through the loss of either mRNA or protein expression. However, the molecular mechanisms underlying its dysregulation have not been fully explored. Interleukin-6 (IL-6) mediated Stat3 activation is viewed as crucial for multiple tumor growth and progression. Here, we demonstrate that PTPN13 is a direct transcriptional target of Stat3 in the squamous cell lung carcinoma. Our data show that IL-6 administration or transfection of a constitutively activated Stat3 in HCC-1588 and SK-MES-1 cells inhibits PTPN13 mRNA transcription. Using luciferase reporter and ChIP assays, we show that Stat3 binds to the promoter region of PTPN13 and promotes its activity through recruiting HDAC5. Thus, our results suggest a previously unknown Stat3-PTPN13 molecular network controlling squamous cell lung carcinoma development.
    09/2013; 2013:468963. DOI:10.1155/2013/468963
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    ABSTRACT: PTPN13 is a new candidate tumor-suppressing gene. To investigate the PTPN13 expression and its potential function in the invasion and metastasis of lung squamous cell carcinoma (LSCC), we performed this study in 91 primary LSCC tissues and the adjacent non-cancerous tissues. The mRNA expression of PTPN13 and FAK was quantitated by reverse transcription polymerase chain reaction. The protein expression of PTPN13, focal adhesion kinase (FAK) and phosphorylated FAK (P-FAK) was evaluated using immunohistochemical staining and western blotting. The association among PTPN13 expression, FAK expression and the clinicopathological parameters were analyzed. PTPN13 expression was down-regulated in LSCC, and was negatively correlated with the cancer grade and stage. FAK mRNA, as well as FAK protein level was elevated in LSCC tissues. P-FAK level, also found increased, had no association with FAK mRNA and FAK protein expression, but had a negative correlation with the PTPN13 expression. P-FAK level had a significant positive correlation with the TNM classification. The over-expression of FAK and increased FAK phosphorylation plays an important role in the invasion and metastasis of LSCC. PTPN13 may function as an antioncogene via inhibiting the phosphorylation of FAK.
    Experimental and Molecular Pathology 07/2013; 95(3). DOI:10.1016/j.yexmp.2013.07.008 · 2.71 Impact Factor
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    ABSTRACT: Previous studies investigating the association between glutathione S-transferase P1 (GSTP1) Ile105Val polymorphism and bladder cancer risk reported controversial results. This study aimed to quantify the strength of the association between GSTP1 Ile105Val polymorphism and bladder cancer risk by performing a meta-analysis. We searched the PubMed, Embase, and Wanfang databases for publications on the association between GSTP1 Ile105Val polymorphism and bladder cancer risk. We estimated the pooled odds ratios (ORs) with their confidence intervals (95 %CIs) to assess the association. Twenty-five individual studies with a total of 12,360 subjects were finally included. Meta-analysis of all 25 studies showed that GSTP1 Ile105Val polymorphism was associated with increased risk of bladder cancer risk under four genetic comparison models (for G versus A, random-effect OR = 1.19, 95 %CI 1.05-1.35; for GG versus AA, random-effect OR = 1.49, 95 %CI 1.12-1.97; for GG/GA versus AA, random-effect OR = 1.20, 95 %CI 1.03-1.39; for GG versus GA/AA, random-effect OR = 1.41, 95 %CI 1.10-1.80). Sensitivity analysis showed that GSTP1 Ile105Val polymorphism was still associated with bladder cancer risk under three genetic comparison models (for G versus A, random-effects OR = 1.13, 95 %CI 1.01-1.26; for GG versus AA, random-effects OR = 1.29, 95 %CI 1.01-1.65; for GG versus GA/AA, random-effects OR = 1.19, 95 %CI 1.04-1.35). No evidence of publication bias was observed. This meta-analysis shows that there is an obvious association between GSTP1 Ile105ValIle105Val polymorphism and bladder cancer risk, and GSTP1 ILE105VAL polymorphism contributes to bladder cancer risk.
    Tumor Biology 03/2013; 34(3). DOI:10.1007/s13277-013-0698-y · 3.61 Impact Factor
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    ABSTRACT: Objective To investigate the expression and electrophysiological characteristics of purinergic P2X(3) receptors in interstitial cells of Cajal (ICCs) at different time points after partial bladder outlet obstruction (PBOO) in rats. Materials and Methods In all, 48 female Sprague-Dawley rats were randomly divided into four groups: 4, 6 and 8 week PBOO groups and sham-operated controls. At 4 weeks after surgery, cystometry was performed to investigate bladder function in vivo. Subsequently, the rats were humanely killed at 4, 6 or 8 weeks and the bladders were harvested for measurements. P2X(3) expression in ICCs of bladder was investigated by immunofluorescent staining. The level of P2X(3) mRNA was detected by reverse transcription-polymerase chain reaction (RT-PCR). Inward currents in corresponding ICCs after PBOO were investigated electrophysiologically. Results Cystometrography showed a valid increase in maximum detrusor pressure in rats subjected to PBOO. The bladder weight in the PBOO group was significantly higher than that in the control group. In contrast to sham rats, there was a significant increase in the intensity of P2X(3) staining in the ICCs in all PBOO groups. C-kit labelled isolated ICCs were strongly stained with the P2X(3) antibody. RT-PCR showed that the expression of P2X(3) mRNA was significantly up-regulated at 4, 6 and 8 weeks in the ICCs from the PBOO rats. In the ICCs, the mean peak amplitude of inward currents was significantly increased in the PBOO groups compared with the control group. Conclusions The expression of P2X(3) receptors showed a time dependent up-regulation in the ICCs of the bladder in rats with PBOO. PBOO induced the potentiation of P2X(3) receptors function, as evidenced by alpha, beta-methylene ATP-enhanced inward currents in the ICCs of the rat bladder.
    BJU International 08/2012; 111(5). DOI:10.1111/j.1464-410X.2012.11408.x · 3.53 Impact Factor
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    ABSTRACT: To investigate the expression of hyperpolarization-activated cyclic nucleotide-gated (HCN) protein in the interstitial cells of Cajal (ICCs) of the human bladder and to determine the relative expression of the HCN subtypes. A total of 30 bladder specimens were obtained, and each bladder sample was divided into 2 parts. Part I, which included mucosa, submucosa, and muscle, was used for immunofluorescence study. Part II, in which the mucosa and submucosa were removed and fresh bladder muscle tissue was kept, was used for Western blotting. First, the immunoreactivity of HCN1, HCN2, HCN3, and HCN4 isoforms was detected in the ICCs of lamina propria using immunofluorescence. Second, the protein expression of HCN1, HCN2, HCN3, and HCN4 isoforms in ICCs of bladder detrusor muscle was analyzed using Western blotting. Immunofluorescence showed that there were many vimentin- and HCN4-positive ICCs in the lamina propria region and detrusor. Also, only a few c-kit and HCN4-positive ICCs were detected in the lamina propria region and detrusor. Additionally, novel c-kit negative, but HCN4-positive mast cells were found in the lamina propria. Immunofluorescence and Western blotting revealed that HCN1, HCN2, HCN3, and HCN4 channels were all present in the ICCs of the human bladder; however, HCN4 channel expression in the ICCs was greater than in HCN1, HCN2, or HCN3. HCN1, HCN2, HCN3, and HCN4 channels are identified in ICCs of human bladder tissue, and the expression of the HCN4 channel exceeded that of the other subtypes.
    Urology 07/2012; 80(1):224.e13-8. DOI:10.1016/j.urology.2012.04.005 · 2.19 Impact Factor
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    ABSTRACT: Renal ischemia-reperfusion (I/R) injury, as a common and clinically important problem, starts with direct damage caused by chemokines and inflammatory cytokines, which is aggravated by specific and nonspecific immune reactions. Recently, IL-17A has been considered to be in a uniquely powerful position between adaptive and innate immunity. The present study investigated the role of IL-17A in renal I/R injury in mice. We measured the time-course of changes in plasma and renal IL-17A levels using a murine model of renal I/R injury. Then, the protective effect of monoclonal anti-IL-17A antibody, given intravenously at 30 min before or after renal I/R operation, on renal I/R injury was investigated. In addition, the levels of plasma and renal pro- and anti-inflammatory cytokines and chemokines were assessed. IL-17A was significantly increased in plasma and kidneys after renal I/R injury in mice. Furthermore, intravenous administration of neutralizing monoclonal anti-IL-17A antibody attenuated renal I/R injury by evaluating renal function and histopathology. In addition, administration of anti-IL-17A antibody substantially reduced the plasma and renal levels of many pro-inflammatory mediators (TNF-α, IL-6, high-mobility group box 1 (HMGB1), IL-1β, IL-17A, macrophage inflammatory protein-1α (MIP-1α), and monocyte chemoattractant protein-1 (MCP-1), as well as increased the plasma and renal levels of anti-inflammatory cytokines IL-10 and transforming growth factor β (TGF-β). The above data suggest that IL-17A has a detrimental effect on renal I/R injury via facilitating the production of pro-inflammatory cytokines and chemokines as well as hampering the production of anti-inflammatory cytokines.
    Journal of Surgical Research 11/2011; 171(1):266-74. DOI:10.1016/j.jss.2009.12.031 · 1.94 Impact Factor