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Objective To investigate the relationship between the polymorphism of cytochrome P450 19 (CYP19) gene rs10046 and the risk of colon and rectal cancer.Methods Using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) to analyze gene polymorphism in CYP 19 gene rs10046 in 198 cases of colon and rectal cancer patients (case group) and 309 cases of healthy controls (control group).The genotype frequency and relative risk of CYP19 gene rs10046 between the two groups were compared and the relationship with the clinicopathological features of colorectal cancer was analyzed.Results In case group,the prevalence rates of CYP19 rs10046 genotypes C/C,C/T and T/T were 28.3％,44.4％ and 27.3％,respectively,and 17.2％,51.8％ and 31.1％ in the control group,respectively,with statistical significant difference (P ＜ 0.05).Compared with wild-type C/C,the susceptibility of colorectal cancer with the genotypes of C/T and T/T was decreased by 0.521 (95％ CI:0.330-0.822)and 0.532 (95 ％ CI:0.322-0.880) respectively.Moveover,in the non-smoking group,the risk of colorectal cancer with genotype T/T or C/T was decreased by 0.409 (95％ CI:0.210-0.798) compared with genotype C/C.The interaction was not exist in smoking group.Conclusions The polymorphism of CYP19 gene rs10046 is related to the susceptibility of colon and rectal cancer.The T/T,C/T genotype of CYP19 rs10046 decrease the risk of colon and rectal cancer,and which might be the protective factor of colon and rectal cancer.
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Colon cancer associated transcript 2 (CCAT2) is found recently an important member of cancer-related long non-coding RNA (lncRNA).Dysregulation of CCAT2 plays a pivotal role in tumor pathophysiological processes,especially in tumourigenesis and progression of digestive system neoplasms,thus,CCAT2 likely represents a novel cancer biomarker or therapeutic target.Elucidation of the molecular mechanisms of CCAT2 will provide a feasible theoretical basis and potential interventional target for the diagnosis and treatment of malignancies.The present review summarizes current evidences of CCAT2 in digestive system neoplasms.
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Objective To investigate the expression of long non-coding RNA NONHSA1254644 in lung adenocarcinoma and its clinical significance.Methods 99 cases of lung adenocarcinoma and the adjacent tissues as well as clinical data was collected.The expression level was detected by quantitative realtime polymerase chain reaction (qRT-PCR).Then the relationship between the expression level and the clinical parameters was analyzed.Cell counting kit-8 (CCK8) was used to investigate its effect of lung adenocarcinoma cell line A549 on proliferation.Results The expression of NONHSA1254644 was down-regulated in lung adenocarcinoma,and its expression was positively correlated with the differentiation of patients.The overexpression of NONHSA1254644 could inhibit the proliferation of A549 cells.Conclusions NONHSA1254644 is involved in the development and progression of lung adenocarcinoma.
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The aberrant expression of MicroRNA-137 (miR-137) is correlated with different tumors closely,miR-137 promoter methylation considered as one of the most important mechanisms through which miR-137 expression can be regulated.The degree of promoter methylation of miR-137 was significantly increased in tumors,but the frequencies varied.In addition,it correlated with different clinical and pathological characteristics in tumors.Furthermore,miR-137 promoter methylation indicated poor prognosis.miR-137 promoter methylation promoted the initiation and progression of tumors,it was of potential to be a biomarker and reversed the methylation status of miR-137 represented a novel strategy of cancer treatment.
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Objective To explore the expressions of glutathione reductase in gastric cancer,to investigate the relationship between glutathione reductase (GSR) and clinical pathological characteristics of gastric cancers,to identify the role of GSR in evaluation of the prognosis of gastric cancer patients,and to investigate the role of GSR in the development of gastric cancer.Methods The gastric cancer datasets were searched and downloaded from The Cancer Genome Atlas (TCGA),and chip data were analyzed with clinical information.Gene set enrichment analysis (GSEA) was conducted to explore the gene sets enriched in samples with high GSR expression.Results The expression of GSR was down-regulated in high grade tumors (P ＜ 0.01).No significant difference was found between different age,Shortest tumor diameter,American Joint Committee on Cancer (AJCC) M stage,Barrett's esophagus,family history of gastric cancer,and Helicobacter pylori (H.pylori) infection.Higher expression of GSR indicated poor prognosis in gastric cancer.GSEA indicated that GSR regulates gene sets associated with oxidative phosphorylation,metabolism of nucleotides,mitochondrial protein import,and mitotic G1 S phases.Conclusions GSR can be used as an indicator to predict the prognosis of gastric cancer patients and a target for the treatment of gastric cancer.
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Objective To investigate the relationship between genetic single-nucleotide polymorphisms of ligase Ⅳ (LIG4) and heat shock protein B1 (HSPB1) and prognosis in nasopharyngeal carcinomas.Methods DNAs were extracted by phenol-chlorofrom method from peripheral blood samples of 168 nasopharyngeal carcinoma patients.Genetic single-nucleotide polymorphisms were divided by Taqman realtime polymerase chain reaction (PCR).All statistical analyses were performed with statistical product and service solutions v13.0.A p-value of less than 0.05 was confirmed as statistical significance.Single-factor and multiple-factor logistic analyses were used to calculate odds ratio (OR) and 95％ confidence interval (CI).Long-rank test and COX were also used.Results No relationship was found between the recurrence,metastasis and overall survival of nasopharyngeal carcinoma and genetic single-nucleotide polymorphisms of LIG4 and HSPB1 with single-factor and multiple-factor logistic analyses.Conclusions LIG4 rs1805388 and HSPB1 rs2868371 had no relationship with prognosis of nasopharyngeal carcinomas.
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Objective To investigate the function and regulatory mechanisms of VCAN gene and protein in metastatic prostate cancer.Methods The data of whole genomic expression profiles got from the prostate cancer metastasis were obtained from gene expression omnibus (GEO) database,a set of bioinformatics tools,such as BRB-Array Tools,protparam,SMART,SignalP 4.0,TMHMM,NetPhos2.0,PredictProtein,SWISS-MODEL,GO,KEGG and STRING softwares were used to accomplish data-mining and bioinformatics analysis.Results There were 73 co-expressed differentially genes in prostate cancer metastasis,21 up-regulated and 52 down-regulated.Bioinformatics analysis indicated that VCAN gene encoded 3396 amino acids,VCAN was also contained one Immunoglobulin domain,two hyaluronan-binding domain,one epidermal growth factor-like domain,one calcium-binding EGF-like domain,one C-type lectin domain and one domain abundant in complement control proteins,and a furthermore analysis suggested that VCAN played essential roles in such important biological function including cell adhesion,hyaluronic acid binding,calcium-binding,glycosaminoglycan binding,extracellular matrix and cell adhesion molecules.Conclusions Bioinformatics analysis had a high efficiency in analyzing microarray data and revealing internal biology information.VCAN may play an important role in the prostate cancer metastasis,Thus,VCAN might be a novel biomarker for the diagnosis of prostate cancer metastasis or a new target for its treatment.
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Objective To understand the molecular aberration at whole genomic level,CGH (comparative genomic hybridization) was used to investigate genetic abnormality in lung cancer.Methods Comparative genomic hybridization was performed in 17 cases to detect the global genomic aberration in cancer tissue cells.Results All of 17 cases detected by CGH showed chromosomal aberrations.The average numbers of chromosomal gains and losses in each case were 7.0 and 4.8 in NSCLC and 8.4 and 9.6 in SCLC,respectively.The frequency of gains and losses on chromosome had no significant differences between NSCLC and SCLC.The frequencies of gains on chromosomal arms 3q24 -28 and 11q13(58.3％ and 58.3％ ) in NSCLC were significantly higher than that in SCLC(0％ and 0％ ) ( P ＜0.05 and ＜0.05,respectively).Conclusions The cytogenetic aberration generally existed in lung cancer cells.Several regions ( more than one) of chromosomal aberration were involved in the carcinogenesis of NSCLC and SCLC.The regions and frequencies of chromosomal aberration in NSCLC were somewhat different from that in SCLC,which might result in the different biological behavior of the two types of lung cancer.The chromosomal aberration might be served as a marker to differentiate the two types of lung cancer.
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Objective To construct an eukaryotic expression vector pEGFP-N1-CKB and establish a stably transfected NCI-H520 cell line.Methods Human CKB gene was amplified by PCR with human CKB cDNA library as the template and the fragment was combined with plasmid pEGFP-N1.The recombinant expression vector,pEGFP-N1-CKB,was transfected to NCI-H520 using Lipofectamin.The stably transfected cell line was established after G418 selection and the expression level of CKB gene before and after transfection was detected by Western blot.Results After identification by restriction enzyme digestion and sequencing,the eukaryotic expression vector,pEGFP-N1-CKB,was successfully constructed.The expression level of CKB in NCI-H520 transfected by pEGFP-N1-CKB was significantly higher than that in control.CKB gene had a stable transfection in NCI-H520 cells.Conclusions An eukaryotic plasmid encoding CKB (pEGFP-N1-CKB) has been constructed and a cell line expressed CKB stably has been successfully prepared.
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Objective To explore the mutation situation of pancreatic cancer cell mitochondria DNA D-loop region. Method PCR and direct sequencing was used to analyze the mutational site of mitochondria DNA D-loop region in two pancreatic cancer cell lines SW1990 and JF-305 and normal primary cultured pancreas cell. Result The point mutations were found in two pancreatic cancer cell lines and normal primary cultured pancreas cell. Eight point mutations were found in SW1990 and 9 point mutations were found in JF-305. Three point mutations (73 site A-G,16223 site C-T, and 16358 site c-T) existed in all two pancreatic cancer cell lines and normal primary cultured pancreas cells, which can be considered as polymorphism. Other two point mutations (16211 site C-T and 16311 site T-C) were only found in two pancreatic cancer cell lines, which can be considered as special mutations. Conclusion The mitochondrial DNA D-loop region of pancreatic cancer cells existed polymorphism and special mutations, and the special mutations might be new molecule marker.
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Objective To explore the relationship between TGF-beta1,BRCA2,HER2,ER,PR and clinical factors in breast cancer.Methods The expression of TGF-beta1,BRCA2,HEB2,ER,PB in 67 cases breast carcinoma were detected by immunohistochemistry staining SP method.The correlation of the results with other parameters which included age,pathohistological grade,status of auxiliary lymph nodes were analyzed by mono-factor unconditional logistic regression analysis.Results The expression of TGF-beta1 was correlated with BRCA2.and the expression of BRCA2 was correlated with TGF-beta1 and c-erbB-2 in breast cancer.Condusion Overexpression of BRCA2 was related with TGF-beta1 and HER2 in breast carcinoma.It was useful in breast carcinoma prognosis by detecting these three factors.
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Objective To explore effects and mechanism of inactivation of vitamin D receptor (VDR) in intestinal tumor growth of APCmin/+ mice. Methods To generate APCmin/+VDR -/- mice through breeding, the number and size of small intestinal and colonic tumors were assessed and compared between APCmin/+ and APCmin/+ VDR -/- mice. The intestinal tumors were diagnosed with HE stain. The expressions of BCL-2,vimentin-1,Stat-1 and MSH-2 proteins of tumors were determined by immanohistocbemistry and compared be-tween APCmin/+ and APCmin/+VDR -/- mice. Results A comparison between APCmin/+ and APCmin/+ VDR -/- mice revealed that the number of the tumors, which were larger than 3mm, was significantly increased in APCmin/+ VDR -/- mice at 4 months of age (P< 0.01). HE staining indicated fistulous adenomas from small intestine and colon of two groups, Immunostaining showed Stat - 1 level in APC-min/+ tumors were increased and MSH-2 and vimentin-1 levels in APCmin/+ VDR-/- mice were increased, compared to APCmin/+tumors. Conclusion These observations suggested that inactivation of VDR promoted the intestinal tumor growth of APCmin/+ mice.
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Objectives Construct a subtractive library of Caski cell line induced by exposing to the space environment by suppression subtractive hybridization and pave the way to explain the molecular mechanisms of the changes at the gene level. Methods Super SMART cDNA synthesis and suppression subtractive hybridization (SSH) were performed to isolate differentially expressed cDNA fragments from strains subclonal 48A9 cell line. cDNA from the 48A9 cell line were used as " tester" , and the other from the control Caski cell line as "driver". Subtractive products were directly inserted into T/A cloning vector, and then transformed into host bacteria to set up a subtractive cDNA library of specially or highly expressed genes in strains subclonal 48A9 cell line. Results mRNA were directly extracted and purified with good quality. Double strand cDNA were reverse transcripted integratedly, and then cut by Rsa I into even length short segments. Liga-tion was identified as high effective. After two hybridizations, a subtractive library of differentially expressed genes in strains subclonal 48A9 cell line was successfully constructed by SSH. Conclusion SSH is an effective approach to isolate differentially expressed genes.
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Objective To explore the clinical significance of expression of DcR3/TR6 gene in the tissue of cardiac cancer and its correlation with survivin gene expression, Methods Two-step immnaohistochemistry technology was adopted to detect the expression of TR6 and survivin gene in 66 cases of cardiac cancer, none of the patients received prior chemotherapy. Results The positive expression rate of TR6 and survivin genes in cardiac cancer was 54.5% and 62.1% , respectively. The expression of TR6 was correlated with histology type,clinical stage and lymph node metastasis of cardiac cancer ( P<0.05 ). The positive expression rate of TR6 in cases that cardiac cancer with survivin expressed was significant higher than those without surviving expressed (χ2=15.145, P<0.01 ). Conclusions The expres-sion of TR6 and survivin can be regarded as valuable indicators for the diagnosis and prognosis of cardiac cancer.