Peng Li

Capital Medical University, Peping, Beijing, China

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Publications (29)53.96 Total impact

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    ABSTRACT: Objective: To assess the efficacy and safety of Moluodan () in treating dysplasia in chronic atrophic gastritis (CAG) patients. Methods: This was a multi-centered, double-blind, randomized controlled trial. The total of 196 subjects were assigned to receive either Moluodan or folic acid in a 2:1 ratio by blocked randomization. Mucosa marking targeting biopsy (MTB) was used to insure the accuracy and consistency between baseline and after 6-month treatment. Primary outcomes were histological score, response rate of pathological lesions and dysplasia disappearance rate. Secondary endpoints included gastroscopic findings, clinical symptom and patient reported outcome (PRO) instrument. Results: Dysplasia score decreased in Moluodan group (P=0.002), signififcance was found between groups (P=0.045). Dysplasia disappearance rates were 24.6% and 15.2% in Moluodan and folic acid groups respectively, no significant differences were found (P=0.127). The response rate of atrophy and intestinal metaplasia were 34.6% and 23.0% in Moluodan group, 24.3% and 13.6% in folic acid group. Moluodan could improve erythema (P=0.044), and bile reflflux (P=0.059), no signifificance between groups. Moluodan was better than folic acid in improving epigastric pain, epigastric suffocation, belching and decreased appetite (P<0.05), with symptom disappearance rates of 37% to 83%. Conclusions: Moluodan improved dysplasia score in histopathology, and erythema and bile reflflux score in endoscopy, and superior to folic acid in improving epigastric pain, epigastric suffocation, belching and decreased appetite. [ChiCTR-TRC-00000169].
    Chinese Journal of Integrative Medicine 10/2015; DOI:10.1007/s11655-015-2114-5 · 1.22 Impact Factor
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    ABSTRACT: Detection of esophageal dysplasia/early esophageal squamous cell carcinoma (ESCC) is essential for improving 5-year survival. The aim of this prospective study was to evaluate whether Lugol chromoendoscopy improves the detection of esophageal dysplasia/early ESCC in patients with esophageal symptoms in a low-incidence region in China. Eligible patients were randomly assigned into two groups who received routine endoscopy or Lugol chromoendoscopy. During endoscopy, between one and five biopsies were taken from visible lesions for routine endoscopy, or unstained areas of >0.5 cm in diameter for Lugol chromoendoscopy. In total, 812 patients were enrolled, 395 for routine endoscopy and 417 for Lugol chromoendoscopy. The overall detection rate of esophageal dysplasia/early ESCC was 10.6% (86/812), the detection rates were 7.3% (29/395) and 13.7% (57/417) in routine and chromoendoscopy groups, respectively (χ(2)=8.58, P=0.003). The detection rates were 8.3% (48/580), 17.2% (17/99) and 16.5% (22/133), respectively, in patients with reflux, dysphagia and globus sensation symptoms. In the chromoendoscopy group, 213 patients had unstained lesions of >0.5 cm, the detection rates of dysplasia/early carcinoma were 5.3% (4/76) in those with lesions of 0.5-1.0 cm, and 37.2% (51/137) in those with lesions >1.0 cm (χ(2)=21.46, P<0.001). These results indicate that Lugol chromoendoscopy improves the detection rate of esophageal dysplasia/early carcinoma in patients with esophageal symptoms compared with routine endoscopy. We propose that Lugol chromoendoscopy must therefore be considered in addition to routine endoscopy in patients with esophageal symptoms.
    Oncology letters 07/2015; 10(1):45-50. DOI:10.3892/ol.2015.3230 · 1.55 Impact Factor
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    ABSTRACT: Esophageal cancer is one of the most common malignant cancers worldwide. The molecular mechanism of esophageal squamous cell carcinoma (ESCC) is still poorly understood. ESE3 is a member of the Ets transcription family, which is only expressed in epithelial tissues and acts as a tumor suppressor gene in prostate cancer. Our study aim was to confirm whether ESE3 is involved in the carcinogenesis of ESCC. Immunohistochemical analysis revealed that ESE3 was mainly located in cell nuclei of normal tissues and the cytoplasm in ESCC tissues. Immunofluorescence and western blot analyses of the normal esophageal cell line HEEpiC and ESCC cell lines EC9706 TE-1, KYSE150, and KYSE410 confirmed these results. pEGFP-ESE3 and pcDNA3.1-V5/HisA-ESE3 plasmids were constructed for overexpression of ESE3 in EC9706 and KYSE150 cells. The stably transfected cells showed restoration of the nuclear localization of ESE3. EC9706 cells with re-localization of ESE3 to the nucleus showed inhibition of proliferation, colony formation, migration, and invasion. To explore the possible mechanism of the differences in localization of ESE3 in normal esophageal cells and ESCC cells, ESCC cell lines were treated with the nuclear export inhibitor leptomycin B, transcription inhibitor actinomycin D, PKC inhibitor sphinganine, P38 MAPK inhibitor SB202190, and CK II inhibitor TBCA. These reagents were chosen according to the well-known mechanisms of protein translocation. However, the localization of ESE3 was unchanged after these treatments. The sequence of ESE3 cDNA in ESCC cells was identical to the standard sequence of ESE3 in the NCBI Genebank database, indicating that there was no mutation in the coding region of ESE3 in ESCC. Taken together, our study suggests that ESE3 plays an important role in the carcinogenesis of ESCC through changes in subcellular localization and may act as a tumor suppressor gene in ESCC, although the mechanisms require further study.
    PLoS ONE 05/2015; 10(5):e0126319. DOI:10.1371/journal.pone.0126319 · 3.23 Impact Factor
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    ABSTRACT: To study the reasons for the discrepancies in pathologic diagnosis of gastric dysplasia/early cancer in endoscopic submucosal dissection (ESD) specimens, and how to cope with the discrepancies. The pathologic diagnoses in 60 cases of ESD specimens according to the three currently used classification systems (namely Western criteria, Japanese criteria and Vienna classification) were compared. The diagnostic discrepancies were analyzed. Fifteen of the 17 cases diagnosed as low-grade intraepithelial neoplasia according to the Western criteria were revised as adenoma by the Japanese criteria. Amongst the 43 cases of gastric intramucosal adenocarcinoma diagnosed according to the Japanese criteria, 23 cases had concordant diagnosis by the Western criteria. While the diagnosis of low-grade intraepithelial neoplasia/adenoma was basically similar irrespective of classification system used, there were significant differences in the interpretation of gastric early cancer. The diagnostic discrepancies in the gastric dysplasia/early cancer are mainly related to the morphologic criteria applied in different classifications. In order to facilitate clinical and pathologic communication, a consensus using Vienna/WHO classifications, supplemented with Japanese system, is desirable.
    Zhonghua bing li xue za zhi Chinese journal of pathology 03/2015; 44(1):21-26.
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    ABSTRACT: Cigarette smoke is a risk factor for esophageal squamous cell carcinoma (ESCC). It contains several carcinogens known to initiate and promote tumorigenesis as well as metastasis. The nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is one of the strongest carcinogens in tobacco and our previous studies have shown its proliferation-promoting role in the progression of ESCC. Recently, NNK was identified as an agonist for both beta1- and beta2-adrenoceptors. Thus, we hypothesized that the cancer-promoting effect of NNK was likely mediated through beta-adrenoceptors in ESCC. Therefore, we investigated the comprehensive role of NNK in ESCC in vitro and in vivo, and found that NNK promoted many oncogenic features including ESCC cell proliferation and xenograft tumor growth as well as ESCC cell migration and invasion. Western blotting showed that NNK induced significant up-regulation of phosphorylated ERK1/2, cyclin D1, Bcl-2, and vascular endothelial growth factor as well as down-regulation of Bax. Importantly, the oncogenic effects of NNK in ESCC and the altered protein expression were reversed to some extent by down-regulation of beta1- and beta2-adrenoceptors with the beta2-adrenoceptor showing a greater rescue effect. Taken together, our in vitro and in vivo results demonstrate that NNK plays an oncogenic role in ESCC through beta-adrenoceptors. Furthermore, beta2-adrenoceptor might play a more important role in this process. Our findings might provide a chemoprevention and therapy strategy for cigarette smoke-related ESCC carcinogenesis.
    PLoS ONE 03/2015; 10(3):e0118845. DOI:10.1371/journal.pone.0118845 · 3.23 Impact Factor
  • Ming Zhang · Peng Li · Xiaoge Zhou
    Zhonghua bing li xue za zhi Chinese journal of pathology 10/2014; 43(10):704-5.
  • Shutian Zhang · Peng Li
    Zhonghua nei ke za zhi [Chinese journal of internal medicine] 07/2014; 53(7):511-2.
  • Zhonghua bing li xue za zhi Chinese journal of pathology 05/2014; 43(5):344-7.
  • Peng Li · Rui Cheng · Shutian Zhang
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    ABSTRACT: To review the advances of studies on clinical results of aspirin's chemopreventive effect against esophageal squamous cell carcinoma (ESCC) and evidences for mechanisms of the antitumoural effects of aspirin in experimental research. A comprehensive search of the PubMed literatures without restriction on the publication date was carried out using keywords such as aspirin and esophageal cancer. Articles associated with aspirin and esophageal cancer are analyzed. This review focuses on the current evidence for use of aspirin as a chemopreventive agent in ESCC. Aspirin is the most widely used among all nonsteroidal anti-inflammatory drugs (NSAIDs), which is cheap and acceptable to patients. Several observational results provide the further investigation of prevention and therapy of aspirin or similar drugs in esophageal cancer. Data from case control studies, cohort studies and randomized controlled trials (RCTs) also give some support of a beneficial role of aspirin on ESCC. Experimental data suggest that aspirin may prevent carcinogenesis of ESCC by favorably affecting proliferation, apoptosis, or other as yet unidentified growth-regulating processes. But the mechanism by which aspirin influence on esophageal squamous cell carcinoma needs further investigation. A wealth of evidences ranging from clinical data to experimental results are building to suggest that aspirin has significant effects in reducing both the incidence and mortality of ESCC.
    Chinese medical journal 04/2014; 127(7):1365-9. DOI:10.3760/cma.j.issn.0366-6999.20140227 · 1.05 Impact Factor
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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; 15(5). DOI:10.1111/1751-2980.12130 · 1.96 Impact Factor
  • Na-Na Zhang · Peng Li · Shu-Tian Zhang
    Chinese medical journal 11/2013; 126(21):4189-4191. · 1.05 Impact Factor
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    ABSTRACT: Esophageal cancer is the sixth leading cause of cancer-related deaths worldwide. It has been reported that histone demethylases are involved in the carcinogenesis of certain types of tumors. Here, we studied the role of one of the histone lysine demethylases, plant homeodomain finger protein 8 (PHF8), in the carcinogenesis of esophageal squamous cell carcinoma (ESCC). Using short hairpin RNA via lentiviral infection, we established stable ESCC cell lines with constitutive downregulation of PHF8 expression. Knockdown of PHF8 in ESCC cells resulted in inhibition of cell proliferation and an increase of apoptosis. Moreover, there were reductions of both anchorage-dependent and -independent colony formation. In vitro migration and invasion assays showed that knockdown of PHF8 led to a reduction in the number of migratory and invasive cells. Furthermore, downregulation of PHF8 attenuated the tumorigenicity of ESCC cells in vivo. Taken together, our study revealed the oncogenic features of PHF8 in ESCC, suggesting that PHF8 may be a potential diagnostic marker and therapeutic target for ESCC.
    PLoS ONE 10/2013; 8(10):e77353. DOI:10.1371/journal.pone.0077353 · 3.23 Impact Factor
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    ABSTRACT: To investigate the role of hepatocye apoptosis and mitochondrial permeability transition pore (MPTP) opening in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Thirty male SD rats were randomized into normal diet group and high-fat diet group. At 4, 8 and 12 week of feeding. The hepatocyte apoptosis index (AI) was measured using flow cytometry, and MPTP opening was evaluated with ultraviolet spectrophotometry. Immunohistochemistry was employed to detect hepatic expressions of Bcl-2 and Bax, and Western blotting was used to detect Bax protein expression changes. High-fat feeding resulted in significantly increased hepatocyte AI at 4-12 weeks and gradually increased MPTP opening. In the high-fat diet group, hepatic Bcl-2 expression was detected but the positive cell number remained stable, whereas Bax-positive cell number increased steadily with time with progressively increased intensity of Bax protein expression, resulting in gradually decreased Bcl-2/Bax ratio. Hepatocyte apoptosis occurs in the rat model of NAFLD in close correlation with mitochondrial damage. Increased MPTP opening as the result of increased Bax expression and aberrant Bcl-2/Bax ratio is an important mechanism of hepatocye mitochondrial damage in NAFLD.
    Nan fang yi ke da xue xue bao = Journal of Southern Medical University 07/2013; 33(7):1062-1066.
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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; 58(5). DOI:10.1007/s10620-012-2429-4 · 2.61 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. DOI:10.1111/j.1751-2980.2012.00578.x · 1.96 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. DOI:10.3748/wjg.v18.i10.1117 · 2.37 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. DOI:10.3748/wjg.v18.i6.532 · 2.37 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. DOI:10.3748/wjg.v17.i41.4572 · 2.37 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. DOI:10.1007/s10620-011-1734-7 · 2.61 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. DOI:10.1111/j.1442-2050.2011.01199.x · 1.78 Impact Factor

Publication Stats

120 Citations
53.96 Total Impact Points


  • 2006–2015
    • Capital Medical University
      • • Department of Gastroenterology
      • • Department of Radiology
      Peping, Beijing, China
  • 2013
    • Luzhou Medical College
      Lu-chou, Sichuan, China