Peng Li

Capital Medical University, Peping, Beijing, China

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Publications (17)37.21 Total impact

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    ABSTRACT: To construct and test a diagnostic model using analysis of serum samples for the diagnosis of gastric precancerous lesions and cancer. This study included 25 patients with gastric precancerous lesions (chronic atrophic gastritis with mild to moderate dysplasia) treated from March 2011 to October 2011 at the Endoscopic Center, Beijng Friendship Hospital, Capital Medical University, and Xiyuan Hospital, Chinese Medicine Research Institute; 25 patients with gastric cancer treated at the Endoscopic Center and Surgery Department, Beijing Friendship Hospital; and 25 healthy control subjects treated at Beijng Friendship Hospital. Fasting venous blood samples were collected from all subjects, and the serum samples were examined using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS). A diagnostic model for detecting gastric precancerous lesions and cancer was constructed and tested. Analysis of the MALDI-TOF-MS results showed that the spectral peaks for the peptides with mass/charge ratios of 1741 and 4210 were the most significantly different among the three groups. These values were used to construct a diagnostic model to differentiate among the three groups. The model detected serum samples from healthy control subjects, patients with gastric precancerous lesions, and patients with gastric cancer with a sensitivity of 80% (12/15), 67% (10/15), and 67% (10/15), and the specificity was 67% (20/30), 73% (22/30), and73% (22/30), respectively. Our diagnostic model using serum analysis findings is useful for the diagnosis of gastric precancerous lesions and cancer.
    Journal of Digestive Diseases 01/2014; · 1.85 Impact Factor
  • Chinese medical journal 11/2013; 126(21):4189-4191. · 0.90 Impact Factor
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    ABSTRACT: BACKGROUND: Heparin-binding growth factor signaling is involved in the pathogenesis and development of human cancers. It can be regulated by sulfation of cell-surface heparan sulfate proteoglycans (HSPG). SULF1 is a heparin-degrading endosulfatase which can modulate the sulfation of HSPGs. AIM: The purpose of this study was to elucidate the role of SULF1 in modulating proliferation and invasion of esophageal squamous cell carcinoma (ESCC) by decreasing heparin-binding growth factor signaling. METHODS: We restored SULF1 expression in the ESCC cell line KYSE150, and examined the effects of SULF1 expression on the proliferation and invasion of KYSE150 cells. In addition, we investigated the expression of SULF1 in human ESCC tissues and analyzed the correlation of SULF1 expression with clinicopathologic characteristics of ESCC. RESULTS: Our study shows that re-expression of SULF1 in ESCC cell line results in the downregulation of hepatocyte growth factor-mediated activation of MAPK pathways with a resultant decrease in cell invasiveness. Cell proliferation was also inhibited in SULF1-transfected KYSE150 cells. Immunohistochemical assays reveal that SULF1 is expressed in nearly half of the human ESCC tissues but not in normal esophageal epithelial cells. SULF1 expression in human ESCC tissues is negatively correlated with tumor size and tumor invasion. CONCLUSION: This study identified that SULF1 inhibits proliferation and invasion of ESCC by decreasing heparin-binding growth factor signaling and suggested that SULF1 plays an inhibiting role in the pathogenesis of ESCC.
    Digestive Diseases and Sciences 10/2012; · 2.26 Impact Factor
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    ABSTRACT: Cigarette smoke extracts (CSE) could promote esophageal squamous cell carcinoma (ESCC) through upregulation of cyclooxygenase-2 (COX-2) expression. Promoter methylation mediates the transcriptional modulation of the COX-2 gene. The aim of the study was to explore whether COX-2 promoter methylation regulated COX-2 expression and functional activity in ESCC exposed to CSE. The methylation status of COX-2 promoter in two human ESCC cell lines, EC109 and TE-1, was examined using bisulfite sequencing analysis. COX-2 mRNA and protein expression were detected by reverse-transcription polymerase chain reaction and Western blot. Prostaglandin E₂ (PGE₂) was examined by enzyme linked immunosorbent assay (ELISA). The promoter was hypermethylated in TE-1 which had a low level of COX-2 expression and was hypomethylated in EC109 with a relatively high level of COX-2 expression. Stimulation by cigarette smoke ethanol extract (EE) resulted in increased COX-2 expression in EC109, but not in TE-1. Treatment with 5-aza-2'-deoxycytidine (5-aza-DC) demethylated the promoter and upregulated COX-2 expression as well as PGE(2) production in TE-1, especially followed by EE stimulation. No significant effect was observed in EC109. These findings suggest that promoter methylation may be one of the mechanisms regulating COX-2 expression in ESCC in response to stimulation of CSE.
    Journal of Digestive Diseases 04/2012; 13(4):208-13. · 1.85 Impact Factor
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    ABSTRACT: To investigate the association between the polymorphism of TBX21 gene and the risk of gastric cancer in a Chinese population. The -1993 polymorphism located in TBX21 gene promoter region was identified by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. The risk between TBX21 gene genotype and gastric cancer was determined by multivariate logistic regression analysis in 220 gastric cancer patients and 262 cancer-free controls matched by age, sex and ethnicity. Compared with the TBX21 -1993TT genotype, the -1993CC genotype exhibited a significantly elevated risk for gastric cancer [Odds ratio (OR) = 3.42, 95% confidence interval (CI): 1.41-8.31]. The relationship between the -1993 polymorphic genotype and the invasive status such as lymph node and distant metastasis was found among the gastric cancer patients (OR = 4.02, 95% CI: 1.87-8.66; OR = 7.02, 95% CI: 3.44-14.34, respectively). TBX21 -1993 polymorphism might contribute to the risk of gastric cancer, especially to the distant metastasis.
    World Journal of Gastroenterology 03/2012; 18(10):1117-22. · 2.55 Impact Factor
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    ABSTRACT: To investigate the expression and methylation status of the secreted frizzled-related protein 2 (SFRP2) in esophageal squamous cell carcinoma (ESCC) and explore its role in ESCC carcinogenesis. Seven ESCC cell lines (KYSE 30, KYSE150, KYSE410, KYSE510, EC109, EC9706 and TE-1) and one immortalized human esophageal epithelial cell line (Het-1A), 20 ESCC tissue samples and 20 paired adjacent non-tumor esophageal epithelial tissues were analyzed in this study. Reverse-transcription polymerase chain reaction (RT-PCR) was employed to investigate the expression of SFRP2 in cell lines, primary ESCC tumor tissue, and paired adjacent normal tissue. Methylation status was evaluated by methylation-specific PCR and bisulfite sequencing. The correlation between expression and promoter methylation of the SFRP2 gene was confirmed with treatment of 5-aza-2'-deoxycytidine. To assess the potential role of SFRP2 in ESCC, we established stable SFRP2-transfected cells and examined them with regard to cell proliferation, colony formation, apoptosis and cell cycle in vivo and in vitro. SFRP2 mRNA was expressed in the immortalized normal esophageal epithelial cell line but not in seven ESCC cell lines. By methylation-specific PCR, complete methylation was detected in three cell lines with silenced SFRP2 expression, and extensive methylation was observed in the other four ESCC cell lines. 5-aza-2'-deoxycytidine could restore the expression of SFRP2 mRNA in the three ESCC cell lines lacking SFRP2 expression. SFRP2 mRNA expression was obviously lower in primary ESCC tissue than in adjacent normal tissue (0.939 ± 0.398 vs 1.51 ± 0.399, P < 0.01). SFRP2 methylation was higher in tumor tissue than in paired normal tissue (95% vs 65%, P < 0.05). The DNA methylation status of the SFRP2 correlated inversely with the SFRP2 expression. To assess the potential role of SFRP2 in ESCC, we established stable SFRP2 transfectants and control counterparts by introducing pcDNA3.1/v5 hisA -SFRP2 or pcDNA3.1/v5 hisA -empty vector into KYSE30 cells lacking SFRP2 expression. After transfection, the forced-expression of SFRP2 was confirmed by the RT-PCR. In comparison with the control groups, stably-expressed SFRP2 in KYSE 30 cells significantly reduced colony formation in vitro (47.17% ± 15.61% vs 17% ± 3.6%, P = 0.031) and tumor growth in nude mice (917.86 ± 249.35 mm(3)vs 337.23 ± 124.43 mm(3), P < 0.05). Using flow cytometry analysis, we found a significantly higher number of early apoptotic cells in SFRP2-transfected cells than in the control cells (P = 0.025). The mean cell number in the S and G2-M phases of the cell cycle was also significantly lower in SFRP2-transfected KYSE30 cells compared with mock transfected counterparts. Silencing of SFRP2 expression through promoter hypermethylation may be a factor in ESCC carcinogenesis through loss of its tumor-suppressive activity.
    World Journal of Gastroenterology 02/2012; 18(6):532-40. · 2.55 Impact Factor
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    ABSTRACT: To study the relationship between the cyclooxygenase (COX)-2 gene and the proliferation and apoptosis of esophageal squamous carcinoma EC109 cells. The techniques of RNA interference (RNAi) and cell transfection, as well as the levels of oncogenicity in nude mice, were used to study the role of COX-2 in the esophageal squamous carcinoma cell (ESCC) line EC109. Following RNAi and transfection, Western blotting analysis was used to determine the expression of the COX-2 protein. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) reduction assay was used to evaluate cell growth, and flow cytometry was used to detect cell apoptosis. Western blotting analysis demonstrated that COX-2 expression was significantly reduced in EC109 cells treated with COX-2-specific short interfering RNA (siRNA) but was increased in EC109 cells transfected with COX-2. Furthermore, COX-2 siRNA treatment inhibited cell proliferation (P < 0.01) and induced apoptosis in EC109 cells, as determined by an MTT assay and by flow cytometry, respectively. In contrast, transfected COX-2 led to increased cell proliferation (P < 0.05) and decreased apoptosis in EC109 cells. In addition, combination treatment of cells with COX-2 siRNA and aspirin had a synergistic effect (P < 0.01). For experiments measuring tumorigenicity, xenograft tumors of a greater volume and weight were found in the COX-2 group compared with other groups (P < 0.05). A large dose of aspirin inhibited tumor growth in nude mice effectively (P < 0.05), and the rate of tumor suppression was 51.8% in the high-dose aspirin group. COX-2 plays a very critical role in ESCC carcinogenesis, and COX-2 siRNA combined with aspirin has the potential to be an anticancer therapy for the treatment of ESCC.
    World Journal of Gastroenterology 11/2011; 17(41):4572-80. · 2.55 Impact Factor
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    ABSTRACT: The secreted frizzled-related protein 1 (SFRP1) gene, as a Wnt signaling modulator, is frequently inactivated by promoter methylation in many tumors including gastric cancer, breast cancer, oral squamous cell carcinoma, and esophageal adenocarcinoma. However, the role of SFRP1 in esophageal squamous cell carcinoma (ESCC) is not clear. In this study, we investigated the epigenetic inactivation of the SFRP1 gene in ESCC. Nine ESCC cell lines, two immortalized human esophageal epithelial cell lines, twenty ESCC tissues, and paired adjacent nontumor tissues were analyzed in the study. Methylation-specific polymerase chain reaction (PCR), bisulfite sequencing, reverse-transcription PCR, immunohistochemistry, and chromatin immunoprecipitation assay were used to detect SFRP1 promoter methylation, expression of the SFRP1 gene, and histone modification in the SFRP1 promoter region. The SFRP1 promoter was found to be highly methylated in 95% (19/20) of the ESCC tissues and in nine ESCC cell lines, compared with 65% (13/20) of the paired nontumor tissues. Moreover, we confirmed that complete methylation of the SFRP1 gene promoter was correlated with its greatly reduced expression level. After individual treatment with 5-aza-2'-deoxycytidine (DAC) and trichostatin A (TSA), the messenger RNA (mRNA) level of the SFRP1 gene was not obviously rescued in the EC9706 cell line. Combined incubation with DAC and TSA can, however, substantially increase the SFRP1 mRNA expression level in the EC9706 cell line. Chromatin immunoprecipitation assay showed that acetylated histone H3 and H4 were found in the SFRP1 promoter region. Promoter hypermethylation of SFRP1 is a frequent event in ESCC. Promoter methylation and histone acetylation may cooperatively regulate expression of the SFRP1 gene.
    Digestive Diseases and Sciences 05/2011; 56(11):3195-203. · 2.26 Impact Factor
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    ABSTRACT: To explore the role of DNA methyltransferase 1 (DNMT1) in esophageal squamous cell carcinoma (ESCC) and the potential of DNMT1-targeted small interfering RNA as ESCC therapy, we examined expression changes of DNMT1 in ESCC and investigated the effect of DNMT1 knockdown by RNA interference in a human ESCC cell line, KYSE30. DNMT1 messenger RNA was over-expressed in seven out of 12 ESCC samples, and the percentage of cells expressing DNMT1 was significantly higher in ESCC tissues compared with paired non-cancerous tissues. DNMT1 protein levels correlated with lymph node metastasis, but exhibited no correlation with sex, age, tumor site, or tumor differentiation. Knockdown of DNMT1 in KYSE30 cells using RNA interference resulted in a reduction of promoter methylation and re-expression of methyl-guanine methyl-transferase and retinoic acid receptors beta, inhibition of cell proliferation/viability and induction of cell apoptosis. These results indicate that DNMT1 over-expression is involved in ESCC and correlated with lymph node metastasis. Knockdown of DNMT1 led to promoter demethylation and re-expression of several tumor suppressor genes thereby inhibiting cell proliferation/viability and inducing cell apoptosis.
    Diseases of the Esophagus 05/2011; 24(8):601-10. · 1.64 Impact Factor
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    ABSTRACT: Superwarfarins are a class of rodenticides. Gastrointestinal hemorrhage is a fatal complication of superwarfarin poisoning, requiring immediate treatment. Here, we report a 55-year-old woman with tardive upper gastrointestinal hemorrhage caused by superwarfarin poisoning after endoscopic cold mucosal biopsy.
    World Journal of Gastroenterology 04/2010; 16(13):1680-2. · 2.55 Impact Factor
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    ABSTRACT: To study characteristics of collateral circulation of gastric varices (GVs) with 64-row multidetector computer tomography portal venography (MDCTPV). 64-row MDCTPV with a slice thickness of 0.625 mm and a scanning field from 2 cm above the tracheal bifurcation to the lower edge of the kidney was performed in 86 patients with GVS diagnosed by endoscopy. The computed tomography protocol included unenhanced, arterial and portal vein phases. The MDCTPV was performed on an AW4.3 workstation. GVs were classified into three types according to Sarin's Classification. The afferent and efferent veins of each type of GV were observed. The afferent venous drainage originated mostly from the left gastric vein alone (LGV) (28/86, 32.59%), or the LGV more than the posterior gastric vein/short gastric vein [LGV > posterior gastric vein/short gastric vein (PGV/SGV)] (22/86, 25.58%), as seen by MDCTPV. The most common efferent venous drainage was via the azygos vein to the superior vena cava (53/86, 61.63%), or via the gastric/splenorenal shunt (37/86, 43.02%) or inferior phrenic vein (8/86, 9.30%) to the inferior vena cava. In patients with gastroesophageal varices type 1, the afferent venous drainage of GV mainly originated from the LGV or LGV > PGV/SGV (43/48, 89.58%), and the efferent venous drainage was mainly via the azygos vein to the super vena cava (43/48, 89.58%), as well as via the gastric/splenorenal shunt (8/48, 16.67%) or inferior phrenic vein (3/48, 6.25%) to the inferior vena cava. In patients with gastroesophageal varices type 2, the afferent venous drainage of the GV mostly came from the PGV/SGV more than the LGV (PGV/SGV > LGV) (8/16, 50%), and the efferent venous drainage was via the azygos vein (10/16, 62.50%) and gastric/splenorenal shunt (9/16, 56.25%). In patients with isolated gastric varices, the main afferent venous drainage was via the PGV/SGV alone (16/22, 72.73%), and the efferent venous drainage was mainly via the gastric/splenorenal shunt (20/22, 90.91%), as well as the inferior phrenic vein (3/23) to the inferior vena cava. MDCTPV can clearly display the afferent and efferent veins of all types of GV, and it could provide useful reference information for the clinical management of GV bleeding.
    World Journal of Gastroenterology 02/2010; 16(8):1003-7. · 2.55 Impact Factor
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    ABSTRACT: To study the liver and spleen volume variations in hepatic fibrosis patients at different histopathological stages. Multidetector computed tomography (MDCT) scan was performed in 85 hepatic fibrosis patients. Liver volume (LV) and spleen volume (SV) were measured. Fifteen healthy individuals served as a control group (S0). The patients were divided into stage 1 (S1) group (n = 34), stage 2 (S2) group (n = 25), stage 3 (S3) group (n = 16), and stage 4 (S4) group (n = 10) according to their histopathological stage of liver fibrosis. The LV and standard LV(SLV)had a tendency to increase with the severity of fibrosis, but no statistical difference was observed in the 5 groups (LV: F = 0.245, P = 0.912; SLV: F = 1.902, P = 0.116). The SV was gradually increased with the severity of fibrosis, and a statistically significant difference in SV was observed among the 5 groups (P < 0.01). The LV/SV ratio and SLV/SV ratio were gradually decreased with the aggravation of hepatic fibrosis, and statistically significant differences in both LV/SV and SLV/SV were found among the 5 groups (P < 0.01). The absence of obvious LV reduction in patients with chronic liver disease may be a morphological index of patients without liver cirrhosis. The SV is related to the severity of fibrosis, and the spleen of patients with advanced fibrosis is enlarged evidently. The LV/SV ratio and SLV/SV ratio are of a significant clinical value in the diagnosis of advanced liver fibrosis.
    World Journal of Gastroenterology 07/2009; 15(26):3298-302. · 2.55 Impact Factor
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    ABSTRACT: The biosurfactant is used as the template to synthesize lithium iron phosphate (LiFePO4) precursor with the co-precipitation method and the microwave sintering method is used to prepare positive electrode material LiFePO4 for the lithium ion battery. By using the Brunauer–Emmett–Teller (BET) surface areas, X-ray diffraction (XRD), Fourier transform infrared spectroscopy (FTIR) and conductometer, the authors explored the influence of the microwave power on the structure and performance of the materials. The results the authors got have proved that good crystal and high conductivity values can be obtained from the LiFePO4 powders which are processed 10min under the microwave power of 300W.
    Journal of Alloys and Compounds 03/2009; 471(1):536-538. · 2.73 Impact Factor
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    ABSTRACT: The present study aimed to delineate the actions of cigarette smoke extracts on esophageal squamous-cell carcinoma cell growth in vitro. Both chloroform- and ethanol-extracts from cigarette smoke stimulated human esophageal squamous carcinoma EC109 cell proliferation. Chloroform- and ethanol-extracts also upregulated beta-adrenoceptors expression in EC109 cells. Cyclo-oxygenase-2 (COX-2) expression was increased by chloroform-extract. The stimulatory actions of chloroform-extract on cell proliferation and COX-2 expression were abolished by beta(1)- and beta(2)-adrenoceptor selective antagonists, implicating that COX-2 was downstream to the beta-adrenoceptors. Collectively, the promoting action of chloroform-extract from cigarette smoke on esophageal squamous-cell carcinoma cell proliferation is beta-adrenoceptor- and COX-2-dependent.
    Drug and Chemical Toxicology 02/2009; 32(3):175-81. · 1.29 Impact Factor
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    ABSTRACT: Layered iron phosphate with uniform morphology has been synthesized by a precipitation method with yeast cells as a biosurfactant. The yeast cells are used to regulate the nucleation and growth of layered iron phosphate. The uniform layered structure is characterized by small-angle x-ray diffraction (SAXD), scanning electron microscopy (SEM) and atomic force microscopy (AFM) analyses. Fourier transform infrared spectroscopy (FT-IR) is used to analyze the chemical bond linkages in organic–inorganic hybrid iron phosphate. The likely synthetic mechanism of nucleation and oriented growth is discussed. The electrical conductivity of hybrid iron phosphate heat-treated at different temperatures is presented.
    Smart Materials and Structures 11/2008; 17(6):065034. · 2.02 Impact Factor
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    ABSTRACT: Cigarette smoking has been verified as the risk factor of esophageal squamous cell carcinoma (ESCC). Overexpression of cyclooxygenase 2 (COX-2) is shown in ESCC. The objective of this study was to investigate the effects of cigarette smoking ethanol extract (EE) on the proliferation of the human ESCC cell lines, and to explore the correlation between the proliferation rate of human ESCC cell lines and the expression pattern of COX-2. Whether aspirin can inhibit the proliferation of the ESCC cell lines pretreated with EE, and regulate the mRNA expression levels of COX-2 are also examined. Two human ESCC cell lines were selected. EC109 was poorly differentiated and EC9706 was highly differentiated. EC109 and EC9706 were treated with EE and aspirin for different time course. The cell growth of ESCC was measured by MTT reduction assay and the expression of COX-2 was measured by RT-PCR and Western blot analysis. EE promoted the proliferation of EC109 and EC9706 in dose- and time-dependent manners. In the concentration range (10 - 100 microg/ml for EE) and in the time range (24 - 72 hours) after addition of EE, the cell proliferation was prominent in an up-scaled manner respectively. Aspirin could inhibit the proliferation of cell lines EC109 and EC9706, pretreated with EE for 5 hours, in a dose-dependent manner. In the concentration range (0.5 - 8.0 mmol/L for aspirin), the cell growth inhibition was prominent in an up-scaled manner accordingly (P < 0.05). The effect of EE on cell proliferation was correlated with the up-regulation of COX-2 gene. However, the cell growth inhibition of aspirin was correlated with the down-regulation of COX-2 gene. EE can stimulate the proliferation of human ESCC cell lines EC109 and EC9706, most likely through up-regulating the expression of COX-2. Aspirin can inhibit the proliferation of ESCC cell lines induced by EE, which suggests it may be advantageous in the chemoprevention and therapy of human tobacco-related ESCC. And its effect is likely to be related with modulating COX-2 activity.
    Chinese medical journal 12/2007; 120(23):2086-91. · 0.90 Impact Factor
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    ABSTRACT: In the present study, patch clamp experiments demonstrated the expression of multiple ionic currents, including a Ba2+-sensitive inward rectifier K+ current (IKir), a 4-aminopyridine- (4-AP) sensitive delayed rectifier K+ current (IKDR), and a nifedipine-sensitive, tetrodotoxin-resistant inward Na+ current (INa.TTXR) in the non-transformed rat gastric epithelial cell line RGM-1. RT-PCR revealed molecular identities of mRNAs for the functional ionic currents, including Kir1.2 for IKir, Kv1.1, Kv1.6, and Kv2.1 for IKDR, and Nav1.5 for INa.TTXR. Pharmacologic blockade of Kv and Nav, but not Kir, suppressed RGM-1 cell proliferation. To further elucidate which subtypes of the ion channels were involved in cell proliferation, RNA interference was employed to knockdown specific gene expression. Downregulation of Kv1.1 or Nav1.5 by RNA interference suppressed RGM-1 cell proliferation. To conclude, our study is the first to delineate the expression of ion channels and their functions as growth modulators in gastric epithelial cells.
    Journal of Cellular Physiology 06/2006; 207(2):437-44. · 4.22 Impact Factor