LRP16 was previously identified as an estrogen-induced gene in breast cancer cells. The responsiveness of LRP16 to estrogen and its functional effects in endometrial cancer （EC） cells are still unclear. Here, we sho...LRP16 was previously identified as an estrogen-induced gene in breast cancer cells. The responsiveness of LRP16 to estrogen and its functional effects in endometrial cancer （EC） cells are still unclear. Here, we show that the mRNA level and promoter activity of the LRP16 gene were significantly increased by 17β-estradiol （E2） in estrogen receptor ot （ERα）-positive Ishikawa human EC cells. Although the growth rate of Ishikawa cells was not obviously affected by ectopic expression of LRP 16, the results of a Transwell assay showed an approximate one-third increase of the invasive capacity ofLRP 16-overexpressing cells. As a result of molecular screening, we observed that the expression of E-cadherin, an essential adhesion molecule associated with tumor metastasis, was repressed by LRP16. Further promoter analyses demonstrated that LRP 16 inhibited E-cadherin transactivation in a dose-dependent manner. However, the inhibition was abolished by estrogen deprivation, indicating that the downregulation of E-cadherin transcription by LRP16 requires ERα mediation. Chromatin immunoprecipitation analyses revealed that the binding of ERα to the E-cadherin promoter was antagonized by LRP 16, suggesting that LRP 16 could interfere with ERα-mediated transcription. These results suggest that the upregulation of LRP 16 by estrogen could be involved in invasive growth by downregulating E-cadherin in human ECs.展开更多
AIM: To determine whether HBV with the same characteristics causes dissimilar mutations in different hosts. METHODS: Full-length HBV genome was amplified and linked with pMD T18 vector. Positive clones were selected b...AIM: To determine whether HBV with the same characteristics causes dissimilar mutations in different hosts. METHODS: Full-length HBV genome was amplified and linked with pMD T18 vector. Positive clones were selected by double-restriction endonuclease digestion (EcoRⅠ and HindⅢ) and PCR. Twenty seven clones were randomly selected from an asymptomatic mother [at two time points: 602 (1 d) and 6022 (6 mo)] and her son [602 (S)], and the phylogenetic and mutational analysis was performed using BioEditor, Clustal X and MEGA software. Potential immune epitopes were determined by the Stabilized Matrix Method (SMM), SMM-Align Method and Emini Surface Accessibility Prediction. RESULTS: All of the 27 sequences were genotype C, the divergence between the mother and son was 0%-0.8%. Compared with another 50 complete sequences of genotype C, the mother and her son each had 13 specific nucleotides that differed from the other genotype C isolates. AA 1-11 deletion in preS1 was the dominant mutation in the mother (14/18). The 1762T/1764A double mutation existed in all clones of the mother, 3 of them were also coupled with G1896A mutation, but none were found in the son.17 bp deletion starting at nucleotide 2330 was the major mutation (5/9) in the son, which caused seven potential HLA class Ⅰ epitopes and one B cell epitope deletion, and produced a presumptive new start codon, downstream from the original one of the P gene. CONCLUSION: The HBV strain in the son came from his mother, and discrepant mutation occurred in the mother and her son during infection.展开更多
AIM： To explore whether polymorphisms of the CYPIA1 and GSTM1 genes are associated with susceptibility of stomach cancer. METHODS： A total of 102 stomach cancer cases and 62 healthy persons were diagnosed by patholo...AIM： To explore whether polymorphisms of the CYPIA1 and GSTM1 genes are associated with susceptibility of stomach cancer. METHODS： A total of 102 stomach cancer cases and 62 healthy persons were diagnosed by pathology in 1998- 2000 in the Qilu Hospital of Shandong University. Gene polymorphisms were detected by the PCR using sequencespecific primers. Data analysis of the case-control study was carried out using the unconditional logistic method. RESULTS： After adjustment for age, sex, educational levels, and occupation, the risk factors for stomach cancer were shown to be smoking, Helicobacter pylori （H pylon）, and presence of the CYPIM G/G and GSTM1O/O genotypes. Interaction was observed between the combined genotypes of either CYPIA1 G/G and GSTM1O/O or Hpyloriinfection, or GSTM1O/O and Hpyloriinfection or smoking. CONCLUSION： Polymorphisms of the CYPIA1 and GSTM1 genes, Hpyloriinfection and smoking are related to susceptibility to stomach cancer.展开更多
基金We sincerely thank Dr Pudi Renuka and Dr Jianjun Zhou at the National Cancer Institute for their critical reading of our manuscript. We thank Dr Eric R Fearon at the University of Michigan in USA for the E-cadherin promoter reporters and Dr Nowata at Kyushu University of Japan for the ERα expression vector. This work was supported by the National Natural Science Foundation of China （30471813, 30572096 and 30670809）, the Beijing Natural Science Foundation of China （5052024 and 7052061） and the Chinese PLANational Science Fund for Distinguished Young Scholars grant （06J017）.
文摘LRP16 was previously identified as an estrogen-induced gene in breast cancer cells. The responsiveness of LRP16 to estrogen and its functional effects in endometrial cancer （EC） cells are still unclear. Here, we show that the mRNA level and promoter activity of the LRP16 gene were significantly increased by 17β-estradiol （E2） in estrogen receptor ot （ERα）-positive Ishikawa human EC cells. Although the growth rate of Ishikawa cells was not obviously affected by ectopic expression of LRP 16, the results of a Transwell assay showed an approximate one-third increase of the invasive capacity ofLRP 16-overexpressing cells. As a result of molecular screening, we observed that the expression of E-cadherin, an essential adhesion molecule associated with tumor metastasis, was repressed by LRP16. Further promoter analyses demonstrated that LRP 16 inhibited E-cadherin transactivation in a dose-dependent manner. However, the inhibition was abolished by estrogen deprivation, indicating that the downregulation of E-cadherin transcription by LRP16 requires ERα mediation. Chromatin immunoprecipitation analyses revealed that the binding of ERα to the E-cadherin promoter was antagonized by LRP 16, suggesting that LRP 16 could interfere with ERα-mediated transcription. These results suggest that the upregulation of LRP 16 by estrogen could be involved in invasive growth by downregulating E-cadherin in human ECs.
基金The Natural Science Foundation of Yunnan Province, No.200300172Hospital Science Foundation of The First People’s Hospital of Yunnan Province (2004)
文摘AIM: To determine whether HBV with the same characteristics causes dissimilar mutations in different hosts. METHODS: Full-length HBV genome was amplified and linked with pMD T18 vector. Positive clones were selected by double-restriction endonuclease digestion (EcoRⅠ and HindⅢ) and PCR. Twenty seven clones were randomly selected from an asymptomatic mother [at two time points: 602 (1 d) and 6022 (6 mo)] and her son [602 (S)], and the phylogenetic and mutational analysis was performed using BioEditor, Clustal X and MEGA software. Potential immune epitopes were determined by the Stabilized Matrix Method (SMM), SMM-Align Method and Emini Surface Accessibility Prediction. RESULTS: All of the 27 sequences were genotype C, the divergence between the mother and son was 0%-0.8%. Compared with another 50 complete sequences of genotype C, the mother and her son each had 13 specific nucleotides that differed from the other genotype C isolates. AA 1-11 deletion in preS1 was the dominant mutation in the mother (14/18). The 1762T/1764A double mutation existed in all clones of the mother, 3 of them were also coupled with G1896A mutation, but none were found in the son.17 bp deletion starting at nucleotide 2330 was the major mutation (5/9) in the son, which caused seven potential HLA class Ⅰ epitopes and one B cell epitope deletion, and produced a presumptive new start codon, downstream from the original one of the P gene. CONCLUSION: The HBV strain in the son came from his mother, and discrepant mutation occurred in the mother and her son during infection.
基金Supported by the Association of Science and Technology of Shandong Province, No. Y97C21057
文摘AIM： To explore whether polymorphisms of the CYPIA1 and GSTM1 genes are associated with susceptibility of stomach cancer. METHODS： A total of 102 stomach cancer cases and 62 healthy persons were diagnosed by pathology in 1998- 2000 in the Qilu Hospital of Shandong University. Gene polymorphisms were detected by the PCR using sequencespecific primers. Data analysis of the case-control study was carried out using the unconditional logistic method. RESULTS： After adjustment for age, sex, educational levels, and occupation, the risk factors for stomach cancer were shown to be smoking, Helicobacter pylori （H pylon）, and presence of the CYPIM G/G and GSTM1O/O genotypes. Interaction was observed between the combined genotypes of either CYPIA1 G/G and GSTM1O/O or Hpyloriinfection, or GSTM1O/O and Hpyloriinfection or smoking. CONCLUSION： Polymorphisms of the CYPIA1 and GSTM1 genes, Hpyloriinfection and smoking are related to susceptibility to stomach cancer.
