Objective To evaluate the therapeutic efficacy and toxicity of oxaliplatin (OXA)-based systemic chemotherapy in patients with advanced hepatocellular carcinoma (HCC).Methods Thirty patients with advanced HCC admitted to our hospital from June 2009 to June 2013 were randomly divided into CapeOX group (15 patients,treated with OXA and capecitabine or CAP)and FOLFOX group (15 pa-tients,treated with OXA and calcium folinate or CF,followed by fluorouracil or 5 -FU).The therapeutic effects were evaluated after two cycles of treatment using the Response Evaluation Criteria in Solid Tumors (RECIST 1 .1 ).Assessment criteria included overall response rate (OR),time to tumor progression (TTP),and overall survival (OS)analyzed by Kaplan-Meier survival curves,as well as the toxicity profile of the combination chemotherapy.Comparison of OR was made by chi-square test;assessment of tumor response and toxicity profile was performed by Mann-Whitney U test;OS and TTP were analyzed by log -rank test.Results In the CapeOX group,the OR was 13.3%,and the mean OS and TTP were 10.4 months and 5.0 months,respectively.In the FOLFOX group,the OR was 6.7%,and the mean OS and TTP were 9.0 months and 4.7 months,respectively.The differences between the two groups had no statistical significance in all three parameters (P=0.543,0.606,and 0.769,respectively).Compared with the FOLFOX group,the CapeOX group had significant-ly lower toxicity rates in gastrointestinal tract and myelosuppression (P=0.006 and 0.002,respectively).Conclusions The OXA-based systemic chemotherapy shows anti-tumor effects for advanced HCC,and there is no significant difference in efficacy between the two regi-mens.Decisions regarding the choice of specific treatment should be based on the patients'clinical conditions.

Objective To investigate the effects of granulocyte colony-stimulating factor on proliferation of adipose-derived adult stromal cells(ADASc) in rats. Methods Sixteen SD rats were randomly divided into G-CSF group( n = 8) and control group( n = 8). The rats were subjected to subcutaneous injections of G-CSF at a dose of The ADASc were separated and cultured. Then: ( 1 ) The surface antigens of the ADASc were analyzed by flow cy- tometry. (2)The growth information of the ADASc were observed in vitro. (3)The generation cycle of the ADASc were investigated with the flow cytometry. Results ( 1 ) Flow cytometic detection of ADASe surface marks showed CD44+CD105-CD31-CD45-(2)The doubling generation time, the maximum proliferation multiple and the cell cycle distri- bution of ADASc in G-CSF group had significant difference from that of the control group. Conclusion The discrep- ancy adherence was a practical method to culture the ADASc;G-CSF treatment could promote ADASc re-entering into cell cycle.

0.05).Conclusion The reduction of neoronal proliferation in dentate gyrus may be responsible for the damage of learning and memory ability in aged rats.

Objective To design and construct a controlled adenovirus vector in degradating by itself after induction for solving the problem of stimulating host immune and producing replication adenovirus and providing a secure exogenous gene vectors for clinical practice. Methods Based on the traditional adenovirus vector AdEasyTM system, we inserted the Cre gene which belongs to Cre-LoxP system into the downstream of Tet-On inducible expression system. Two LoxP sites were inserted into two sides of the shuttle plasmid′s right arm genome. Then, the full-length human insulin gene was inserted HindIII enzyme site. After the recombinant adenovirus infected the rat bone marrow-derived mesenchymal stem cells , fluorescent protein expression and insulin secretion were detected before or after induction by Dox. Results A new controlled recombinant adenovirus vector carrying human insulin gene was constructed successfully, and was named AdEasyN/INS. After the transfection of this new vector into QBI-293A cells and rat bone marrow mesenchymal stem cells , green fluorescent protein could be observed. After induction by Dox, both of the ratio of fluorescent cells/total cell and the levels of insulin significantly decreased. Conclusion Construction and preliminary validation of a controlledrecombinant adenovirus vector carrying human insulin gene is constructed successfully , it could infect rat bone marrow mesenchymal stem cells, and degradate by itself after Dox induction, realize the controllability of exogenous gene carrier.

OBJECTIVETo investigate the possible biological function and mechanism of miR-143 in the metastasis of human nasopharyngeal carcinoma (NPC).

METHODSUsing bioinformatics to predict the target gene of miR-143, the 3'UTR and mutant 3'UTR of GLI3 gene was cloned into psiCHECK-2 vector. Dual-luciferase reporter gene assay was employed to examine the repression of the GLI3 gene. miR-143 and GLI3 expression levels in 5-8F cells transfected with miR-143 mimics, inhibitor, or siGLI3 were examined, and the changes in the cell migration ability was assessed by Transwell invasion assay.

RESULTSBioinformatics prediction indicated the Hh pathway transcription gene GLI3 as a target gene of miR-143, and dual-luciferase reporter assay showed that miR-143 directly combined with the 3'UTR of GLI3. qRT-PCR and Western blotting demonstrated that the expression of miR-143 in 5-8F cells was negatively correlated to GLI3 and suppressed the migration of 5-8F cells.

CONCLUSIONMiR-143 can inhibit the invasion of NPC cells by negative regulation of GLI3 gene, which sheds light on the role of miR-143 and Hh pathway in NPC.

Carcinoma ; Cell Line, Tumor ; Cell Movement ; genetics ; Cell Proliferation ; Gene Expression Regulation, Neoplastic ; Genes, Reporter ; Humans ; Kruppel-Like Transcription Factors ; genetics ; MicroRNAs ; genetics ; Nasopharyngeal Neoplasms ; genetics ; pathology ; Nerve Tissue Proteins ; genetics ; Zinc Finger Protein Gli3

OBJECTIVETo detect miR-143 expression in human nasopharyngeal carcinoma (NPC) cell lines and explore the role of miR-143 in regulating the adhesion ability of NPC cells.

METHODSFluorescence quantitative RT-PCR was used to detect miR-143 expression levels in 5 NPC cell lines (CEN1, CNE2, HONE1, 5-8F, and 6-10B) and an immortalized human nasopharyngeal epithelial cell line (NP69). The retrovirus plasmid pMSCV-puro-miR-143 was constructed and the packaged retroviruses pMSCV-puro and pMSCV-puro-miR-143 were infected in 5-8F cells to establish a cell line with stable miR-143 overexpression, whose adhesion ability was tested with adhesion assay.

RESULTSThe expression of miR-143 was down- regulated in the NPC cell lines, and the highly metastatic NPC cell line 5-8F had a expression of only 3.0% of the control level, as compared with the level of 63.59% in the tumorigenic but nonmetastatic NPC cell line 6-10B. The transfected 5-8F cells showed a 1080-fold increase of miR-143 expression (P<0.05) with a significantly lowered adhesion ability.

CONCLUSIONmiR-143 plays a role in regulating the invasiveness and metastasis of NPC, and overexpression of miR-143 causes a significant reduction of the adhesion ability of the highly metastatic NPC cell line 5-8F.

Carcinoma ; Cell Adhesion ; Cell Line, Tumor ; Cell Movement ; Humans ; MicroRNAs ; metabolism ; Nasopharyngeal Neoplasms ; metabolism ; pathology