ABSTRACT
The implementation of cancer genome scientific program has promoted the diagnosis, prevention and tar-get treatment of diseases at molecular level with massive cancer genome data accumulated. Effective mining and use of cancer genome data have thus become the focus in the field of cancer genome. The cancer genome was annotated and demonstrated according to the mining of high-throughput cancer genome data from American National Cancer Research Center, namely the disease-named entity and drug-named entity were identified from the gene function descriptive text and the mined high-throughput data were annotated from their clinical application, in order to help scientific workers to find the relationship between diseases, drugs and genes in scientific literature.
ABSTRACT
A data link-based information aggregation model was established by analyzing the dimensions, approaches, model and its application scope of case specific information aggregation according to the link between information characteristics and the link between information use processes followed by a substantial evidence analysis of information aggregation with Middle East Respiratory Syndrome as an example, which showed that the model can be used in case analysis of health field.
ABSTRACT
Objective To investigate whether emodin enhances chemosensitivity of pancreatic cancer cells and the mechanism. Methods Normal human skin fibroblasts and pancreatic BXPC-3 cells were divided into control group, cisplatin (5 mg/L) treatment group, gemcitabine (0.5 μmol/L) treatment group, emodin (50 μmol/L)+ cisplatin (5 mg/L) co-treatment group and emodin (50 μmol/L) + gemcitabine (0.5 μmol/L) co-treatmentgroup. The cell viability was detected by MTT assay, the cell apoptosis rate by flow cytometry, the expression of the multidrug resistance-associated protein 1 ( MRP1 ), MRP2, breast cancer resistance protein (BCRP) and P-glycoprotein (P-gp) mRNA in different cell lines was determined by reverse transcription polymerase chain reaction.All data were analyzed using the t test. Results The cell viability and apoptosis rate of pancreatic BXPC-3 cells after treatment were 62.44% ± 3.42% and 27. 10% ± 4.24% in the cisplatin treatment group, and they were 30.53% ±0.05% and 66.33% ±9.37% in the emodin + cisplatin co-treatment group. There were significant differences in cell viability and apoptosis rate between the two groups (t = 13.20, 5. 35, P < 0.05 ). The cell viability and apoptosis rate of pancreatic BXPC-3 cells after treatment were 79.82% ±2.83% and 13.48% ± 1.65%in the gemcitabine treatment group, and they were 45.65% ± 2.46% and 62.74% ± 10. 18% in the emodin +gemcitabine co-treatment group. There were significant differences in cell viability and apoptosis rate between the two groups (t = 12.89, 8.28, P < 0. 05 ). There was no significant difference in the viability of normal human skin fibroblasts between the cisplatin treatment group and the emodin + cisplatin co-treatment group, and also between the gemcitabine treatment group and the emodin + gemcitabine co-treatment group (t = 2. 08, 0. 64, P >0.05 ). Expression of MRP1 mRNA was detected in pancreatic BXPC-3 cells, whereas the expression of MRP2,BCRP and P-gp mRNA was undetectable. The expression of MRP1 mRNA in pancreatic BXPC-3 cells was significantly down-regulated in the cisplatin treatment group, and cisplatin + emodin co-treatment had an additive effect on down-regulating the expression of MRP1 mRNA. Conclusion Emodin may enhance chemosensitivity of pancreatic cancer cells to cisplatin by down-regulating the expression of MRP1 mRNA.
ABSTRACT
<p><b>OBJECTIVE</b>To test whether splicing overlapping extension(SOE) method can be a tool for obtaining rare fusion gene's transcripts and to study the tumorigenic capacity of a novel fusion gene AML1-MTG16.</p><p><b>METHODS</b>SOE method was used to obtain AML1- MTG16 fusion gene's transcripts. MTG16, AML1-MTG16 and AML1-MTG16 without III,VI conserved domains of MTG16 segment were inserted into pEGFP- C1,pDsRed-N1 vector respectively,then transfected NIH3T3 cell line by lipofection. Forty-eight hours later, the transfected cells were examined by laser-scanning confocal microscopy. Stable transfected cells were obtained by G418 500ug/ul selection for one month. Growth curve, soft agar colonies formation tumorigenesis in nude mice were done to compare the difference between stable transfected cells.</p><p><b>RESULTS</b>Recombined AML1-MTG16 by SOE contained its CDS. NIH3T3 expressing AML1-MTG16 had a faster proliferation in medium, colony growth in soft agar. AML1-MTG16 expression cells also induced tumors formation following injection into nude mouse. MTG16,AML1-MTG16 and AML1-MTG16 without III,VI conserved domains of MTG16 were colocalized in the nucleus of cotransfected NIH3T3 cells under the examination of laser-scanning confocal microscope.</p><p><b>CONCLUSION</b>SOE is an effective method to get rare fusion gene's transcripts. AML1-MTG16 plays an important role in leukemogenesis. MTG16 may also have a carcinogenic property within the AML1-MTG16 fusion gene. Carcinogenic property of AML1-MTG16 is restricted to its localization in the nuclear matrix. N terminal of MTG16 may play an important part in the carcinogenic activity of AML1-MTG16.</p>