Objective:To study the change of pituitary tumor transforming gene 1 (PTTG1) expression in prostate cancer and its correlation with proliferation and invasion genes.Methods: Patients with prostate cancer who underwent...Objective:To study the change of pituitary tumor transforming gene 1 (PTTG1) expression in prostate cancer and its correlation with proliferation and invasion genes.Methods: Patients with prostate cancer who underwent radical operation in our hospital between March 2015 and January 2018 were selected as the malignant group of the research, and the prostate cancer lesions were collected;patients who underwent transurethral resection of the prostate due to benign prostatic hyperplasia in our hospital during the same period were selected as the benign group of the research, and the benign prostate lesions were collected. The mRNA expression levels of PTTG1, proliferation genes and invasion genes in the lesions were determined. Results:PTTG1, Survivin, Bcl-2, CyclinD1, GPRC6A, ZEB1, CatB, CatD and PAR-1 mRNA expression in prostate cancer lesions of malignant group were significantly higher than those of benign group whereas CDKN2, p21 and TFPI2 mRNA expression were significantly lower than those of benign group;Survivin, Bcl-2, CyclinD1, GPRC6A, ZEB1, CatB, CatD and PAR-1 mRNA expression in prostate cancer lesions with high PTTG1 were significantly higher than those in prostate cancer lesions with low PTTG1 whereas CDKN2, p21 and TFPI2 mRNA expression were significantly lower than those in prostate cancer lesions with low PTTG1.Conclusion:The PTTG1 gene is highly expressed in prostate cancer lesions and it is closely related to the changes of proliferation and invasion gene expression.展开更多
BACKGROUND: Pancreatic cancer is a devastating disease with abnormal genetic changes. The pituitary tumor-derived transforming gene (PTTG) is considered to be implicated in the tumorigenesis of cancers when the gene i...BACKGROUND: Pancreatic cancer is a devastating disease with abnormal genetic changes. The pituitary tumor-derived transforming gene (PTTG) is considered to be implicated in the tumorigenesis of cancers when the gene is epigenetically transformed. In this study, we investigated the relationships between aberrant expression and epigenetic changes of the PTTG1 gene in pancreatic cancer. METHODS: We chose 4 cell lines (PANC-1, Colo357, T3M-4 and PancTu I) and pancreatic ductal adenocarcinoma (PDAC) tissues. After using restriction isoschizomer endonucleases (Msp I /Hpa II) to digest the DNA sequence (5'-CCGG-3'), we performed PCR reaction to amplify the product. And RT-PCR was applied to determine the gene expression. RESULTS: The mRNA expression of the PTTG1 gene was higher in pancreatic tumor than in normal tissue. The gene was also expressed in the 4 PDAC cell lines. The methylation states of the upstream regions of the PTTG1 gene were almost identical in normal, tumor pancreatic tissues and the 4 PDAC cell lines. Some (5'-CCGG-3') areas in the upstream region of PTTG1 were methylated, while some others were unmethylated. CONCLUSIONS: The oncogene PTTG1 was overexpressed in pancreatic tumor tissues and verified by RT-PCR detection. The methylation status of DNA in promoter areas was involved in the gene expression with the help of other factors in pancreatic cancer.展开更多
Objective: To investigate the effect of insulin-like growth factor-1 (IGF-1) on pituitary tumor transforming gene (PTTG) in glioma C6 cells. Methods: Glioma C6 cells were divided into four groups: A group, treated wit...Objective: To investigate the effect of insulin-like growth factor-1 (IGF-1) on pituitary tumor transforming gene (PTTG) in glioma C6 cells. Methods: Glioma C6 cells were divided into four groups: A group, treated without IGF-1; B group, treated with 0.1 ng/mL dose of IGF-1; C group, treated with 1 ng/mL dose of IGF-1; D group, treated with 10 ng/mL dose of IGF-1. PTTG mRNA was detected by reverse transcription polymerase chain reaction (RT-PCR), western blotting was used to detect the expression of PTTG protein. Results: The expressions of PTTG mRNA were 1.370 ± 0.212, 2.198 ± 0.354, 3.452 ± 0.332, and 4.576 ± 0.387 respectively in the four groups, and there was a significantly difference between any two groups (P < 0.01). The protein expressions of PTTG in the four groups were 1.407 ± 0.334, 1.813 ± 0.465, 2.412 ± 0.576, and 3.128 ± 0.665 respectively, and there was a significantly difference between any two groups (P < 0.01). Conclusion: IGF-1 can up-regulate the expression of PTTG significantly in dosage-dependent manner.展开更多
Since the first description of intraductal papillary mucinous neoplasms(IPMNs)of the pancreas in the eighties,their identification has dramatically increased in the last decades,hand to hand with the improvements in d...Since the first description of intraductal papillary mucinous neoplasms(IPMNs)of the pancreas in the eighties,their identification has dramatically increased in the last decades,hand to hand with the improvements in diagnostic imaging and sampling techniques for the study of pancreatic diseases.However,the heterogeneity of IPMNs and their malignant potential make difficult the management of these lesions.The objective of this review is to identify the molecular characteristics of IPMNs in order to recognize potential markers for the discrimination of more aggressive IPMNs requiring surgical resection from benign IPMNs that could be observed.We briefly summarize recent research findings on the genetics and epigenetics of intraductal papillary mucinous neoplasms,identifying some genes,molecular mechanisms and cellular signaling pathways correlated to the pathogenesis of IPMNs and their progression to malignancy.The knowledge of molecular biology of IPMNs has impressively developed over the last few years.A great amount of genes functioning as oncogenes or tumor suppressor genes have been identified,in pancreatic juice or in blood or in the samples from the pancreatic resections,but further researches are required to use these informations for clinical intent,in order to better define the natural history of these diseases and to improve their management.展开更多
Objective: To analysis the chromosome 8 heterozygosity loss in human prostate carcinoma and high grade prostatic intraepithelial neoplasia. Methods: Pure DNA was obtained from prostate neoplasms and normal tissues by ...Objective: To analysis the chromosome 8 heterozygosity loss in human prostate carcinoma and high grade prostatic intraepithelial neoplasia. Methods: Pure DNA was obtained from prostate neoplasms and normal tissues by tissue microdissection. The chromosome 8 heterozygosity loss was detected by PCR based micro-satellite polymorphism analysis technique using 14 pairs of microsatellite primers in 10 samples of prostate carcinoma and 10 samples of high grade prostatic intraepithelial neoplasia. Results: There were different frequencies of chromosome 8 heterozygosity loss in 10 samples of prostate carcinoma. 8p23.1-p23.2 and p21-p22 were two high frequency heterozygosity loss regions. Chromosome 8 heterozygosity loss was detected in 3 samples of high grade prostatic intraepithelial neoplasia. Conclusion: There were high frequency heterozygosity loss regions on chromosome 8 of prostate carcinoma, located at 8p23.1-p23.2 and p21-p22. The high grade prostatic intraepithelial neoplasia and prostate carcinoma share the same allelic loss on 8p. Tumor suppressor genes located at these two regions may be potentially involved in the initiation and progression of prostate carcinoma.展开更多
目的:研究谷胱苷肽S转移酶P1(glutathione S transferase pi,GSTP1)在前列腺癌的表达情况并分析其甲基化状态。方法:采用免疫组织化学方法检测GSTP1在50例前列腺癌石蜡标本中的表达情况,并用甲基化特异性聚合酶链反应(methylation-speci...目的:研究谷胱苷肽S转移酶P1(glutathione S transferase pi,GSTP1)在前列腺癌的表达情况并分析其甲基化状态。方法:采用免疫组织化学方法检测GSTP1在50例前列腺癌石蜡标本中的表达情况,并用甲基化特异性聚合酶链反应(methylation-specific polymerase chain reaction,MSP)方法分析GSTP1基因启动子区5’端CpG岛非甲基化和甲基化的状态。结果:GSTP1在前列腺癌表达的阳性率为18·0%,明显低于癌旁正常前列腺腺体的阳性率(76·0%),P=0·000。GSTP1基因启动子区非甲基化发生率为86%(43/50),50例前列腺癌均未扩增出甲基化特异性产物。结论:GSTP1阴性表达有望成为前列腺癌诊断的一项辅助性新指标。国内前列腺癌GSTP1基因的高频率表达缺失可能与GSTP1基因启动子区甲基化无关,因本组病例数较少,还需进一步积累资料证实。展开更多
基金National Natural Science Youth Science Foundation No:81300626.
文摘Objective:To study the change of pituitary tumor transforming gene 1 (PTTG1) expression in prostate cancer and its correlation with proliferation and invasion genes.Methods: Patients with prostate cancer who underwent radical operation in our hospital between March 2015 and January 2018 were selected as the malignant group of the research, and the prostate cancer lesions were collected;patients who underwent transurethral resection of the prostate due to benign prostatic hyperplasia in our hospital during the same period were selected as the benign group of the research, and the benign prostate lesions were collected. The mRNA expression levels of PTTG1, proliferation genes and invasion genes in the lesions were determined. Results:PTTG1, Survivin, Bcl-2, CyclinD1, GPRC6A, ZEB1, CatB, CatD and PAR-1 mRNA expression in prostate cancer lesions of malignant group were significantly higher than those of benign group whereas CDKN2, p21 and TFPI2 mRNA expression were significantly lower than those of benign group;Survivin, Bcl-2, CyclinD1, GPRC6A, ZEB1, CatB, CatD and PAR-1 mRNA expression in prostate cancer lesions with high PTTG1 were significantly higher than those in prostate cancer lesions with low PTTG1 whereas CDKN2, p21 and TFPI2 mRNA expression were significantly lower than those in prostate cancer lesions with low PTTG1.Conclusion:The PTTG1 gene is highly expressed in prostate cancer lesions and it is closely related to the changes of proliferation and invasion gene expression.
文摘BACKGROUND: Pancreatic cancer is a devastating disease with abnormal genetic changes. The pituitary tumor-derived transforming gene (PTTG) is considered to be implicated in the tumorigenesis of cancers when the gene is epigenetically transformed. In this study, we investigated the relationships between aberrant expression and epigenetic changes of the PTTG1 gene in pancreatic cancer. METHODS: We chose 4 cell lines (PANC-1, Colo357, T3M-4 and PancTu I) and pancreatic ductal adenocarcinoma (PDAC) tissues. After using restriction isoschizomer endonucleases (Msp I /Hpa II) to digest the DNA sequence (5'-CCGG-3'), we performed PCR reaction to amplify the product. And RT-PCR was applied to determine the gene expression. RESULTS: The mRNA expression of the PTTG1 gene was higher in pancreatic tumor than in normal tissue. The gene was also expressed in the 4 PDAC cell lines. The methylation states of the upstream regions of the PTTG1 gene were almost identical in normal, tumor pancreatic tissues and the 4 PDAC cell lines. Some (5'-CCGG-3') areas in the upstream region of PTTG1 were methylated, while some others were unmethylated. CONCLUSIONS: The oncogene PTTG1 was overexpressed in pancreatic tumor tissues and verified by RT-PCR detection. The methylation status of DNA in promoter areas was involved in the gene expression with the help of other factors in pancreatic cancer.
基金the grant of Natural Science Foundation of College and University of Jiangsu Province (No. 05KJD320238).
文摘Objective: To investigate the effect of insulin-like growth factor-1 (IGF-1) on pituitary tumor transforming gene (PTTG) in glioma C6 cells. Methods: Glioma C6 cells were divided into four groups: A group, treated without IGF-1; B group, treated with 0.1 ng/mL dose of IGF-1; C group, treated with 1 ng/mL dose of IGF-1; D group, treated with 10 ng/mL dose of IGF-1. PTTG mRNA was detected by reverse transcription polymerase chain reaction (RT-PCR), western blotting was used to detect the expression of PTTG protein. Results: The expressions of PTTG mRNA were 1.370 ± 0.212, 2.198 ± 0.354, 3.452 ± 0.332, and 4.576 ± 0.387 respectively in the four groups, and there was a significantly difference between any two groups (P < 0.01). The protein expressions of PTTG in the four groups were 1.407 ± 0.334, 1.813 ± 0.465, 2.412 ± 0.576, and 3.128 ± 0.665 respectively, and there was a significantly difference between any two groups (P < 0.01). Conclusion: IGF-1 can up-regulate the expression of PTTG significantly in dosage-dependent manner.
文摘Since the first description of intraductal papillary mucinous neoplasms(IPMNs)of the pancreas in the eighties,their identification has dramatically increased in the last decades,hand to hand with the improvements in diagnostic imaging and sampling techniques for the study of pancreatic diseases.However,the heterogeneity of IPMNs and their malignant potential make difficult the management of these lesions.The objective of this review is to identify the molecular characteristics of IPMNs in order to recognize potential markers for the discrimination of more aggressive IPMNs requiring surgical resection from benign IPMNs that could be observed.We briefly summarize recent research findings on the genetics and epigenetics of intraductal papillary mucinous neoplasms,identifying some genes,molecular mechanisms and cellular signaling pathways correlated to the pathogenesis of IPMNs and their progression to malignancy.The knowledge of molecular biology of IPMNs has impressively developed over the last few years.A great amount of genes functioning as oncogenes or tumor suppressor genes have been identified,in pancreatic juice or in blood or in the samples from the pancreatic resections,but further researches are required to use these informations for clinical intent,in order to better define the natural history of these diseases and to improve their management.
文摘Objective: To analysis the chromosome 8 heterozygosity loss in human prostate carcinoma and high grade prostatic intraepithelial neoplasia. Methods: Pure DNA was obtained from prostate neoplasms and normal tissues by tissue microdissection. The chromosome 8 heterozygosity loss was detected by PCR based micro-satellite polymorphism analysis technique using 14 pairs of microsatellite primers in 10 samples of prostate carcinoma and 10 samples of high grade prostatic intraepithelial neoplasia. Results: There were different frequencies of chromosome 8 heterozygosity loss in 10 samples of prostate carcinoma. 8p23.1-p23.2 and p21-p22 were two high frequency heterozygosity loss regions. Chromosome 8 heterozygosity loss was detected in 3 samples of high grade prostatic intraepithelial neoplasia. Conclusion: There were high frequency heterozygosity loss regions on chromosome 8 of prostate carcinoma, located at 8p23.1-p23.2 and p21-p22. The high grade prostatic intraepithelial neoplasia and prostate carcinoma share the same allelic loss on 8p. Tumor suppressor genes located at these two regions may be potentially involved in the initiation and progression of prostate carcinoma.
