MicroRNAs (MiRNAs) are a contemporary class of short non-coding RNAs,which play a critical role in diverse biological processes, including development, cell proliferation, differentiation, and apoptosis,by suppressing translation of protein coding genes, or cleaving target mRNAs of protein coding genes to induce their degradation. Accordingly, altered miRNA expression is likely to contribute to human disease, including cancer. This review will summarize the emerging knowledge of the association between human miRNA biology and different aspects of carcinogenesis, such as the development, metastesis and therapy strategies.

Object:To investigate the expression of cell cyclin G2 (CCNG2) in glioblastoma tissues and to explore the correla-tion of CCNG2 expression with clinicopathological parameters and clinical significance. Methods:Surgical specimens of glioblastoma were collected from a total of 129 cases. The expression of CCNG2 in 109 specimens with complete clinical data was examined via QRT-PCR and immunohistochemistry. Results:The expression of CCNG2 was significantly decreased in higher stages of glioblastoma compared with those in lower stages. Therefore, CCNG2 is inversely correlated with the stage of the disease. The expression of CCNG2 was associated with tumor stage, sensitivity to chemotherapy and radiotherapy, as well as survival times (P<0.05). CCGN2 was not cor-related with gender and age (P>0.05). Conclusion: CCNG2 expression may be associated with the development, treatment efficacy, and prognosis of glioblastoma. In addition, CCGN2 can be used to evaluate the malignant behavior of glioblastoma.

Objective To investigate the molecular mechanism of peritoneal dissemination of gastric cancer. Methods Literatures in recent years about mechanisms of peritoneal metastasis in gastric cancer were reviewed and summarized.Results Peritoneal metastasis related to viability of cancer cells and peritoneal characteristics. Moreover, it is necessary that many adhesive moleculars, protein hydrolase, cell factors and vascular factors involved in peritoneal metastasis.Conclusion Peritoneal metastasis of gastric cancer was induced by multiple factors together.

Objective To evaluate the clinical effectiveness of the Invance sling in treating children incontinence caused by neurogenic sphincteric incompetence. Methods Two children were treated with Invance sling for their neurogenic sphincteric incompetent incontinence because of congenital myelodysplasia.Both were male,aged of 9 and 10,respectively. Results Two patients were followed up of 12 and 14 months.Both patients micturated once each 2～4 hours with 1～2 episode of incontinence by chance in the daytime and without urinary pad.The maximum bladder capacities were 163 ml and 223 ml pre-operatively and those were 164 ml and 230 ml post-operatively,the retrograde maximum urethral pressures or retrograde leak point pressures were 37 cmH_2O and 27 cmH_2O pre-operatively while those were 45 cmH_2O and 37 cmH_2O post-operatively,maximum urethral closing pressures were 37 cmH_2O and 26 cmH_2O pre-operatively while those were 40 cmH_2O and 37 cmH_2O post-operatively,the functional urethral lengths were 2.5 cm and 3.0 cm pre-operatively while those were 3.5 cm and 4.0 cm post-operatively,the post-voiding residual urine volumes were 40 ml and 30 ml pre-operatively while those were 6 ml and 25 ml post-operatively.Post-operative voiding cystourethrography demonstrated that it was pressed to narrow at the suspended in the bulbous urethra segment. Conclusions The sling in treating children neurogenic sphincteric incompetent incontinence is simple,mini-invasive.It can increase the urethral resistance and continence better.But it has specific indication and should be applied prudently.

Objective To investigate the relationship between galectin-3 and tumour metastasis, and the future prospect of galectin-3 in clinic.Methods Related articles were reviewed. Results Galectin-3, a member of the ?-galactoside-binding proteins, is expressed widely in epithelial and immune cells, and interacts with intracellular glycoproteins, cell surface molecules and extracellular matrix proteins. Galectin-3 is involved in various biological phenomena including cell growth, adhesion, differentiation, angiogenesis and apoptosis, and is associated with invasion and metastasis of tumour. Conclusion Because of the correlation between galectin-3 and tumour invasion and metastasis, galectin-3 may act as the diagnostic marker for tumour metastasis and one of the target proteins for cancer treatment.

The purpose of this study was to investigate the pharmacokinetic interaction between sunitinib and ramipril in rats. Eighteen male SD rats were divided into three groups, with each group being assigned to orally receive sunitinib, ramipril, sunitinib and ramipril, respectively, for ten days. Blood samples were collected at dif-ferent times after first-day and tenth-day administration. The concentrations of ramiprilat and sunitinib in rat plasma were determined by LC/MS/MS and the pharmacokinetic parameters were calculated and statistically analyzed. Compared with the administration of ramipril alone, after a single-dose combined administration, tmax of ramiprilat decreased significantly and t1/2 prolonged, while AUC0-∞ remained unchanged. These results indicated that the ab-sorption rate of ramiprilat increased and the elimination rate decreased, but total absorption degree was not changed. After multiple-dose administrations, CL of ramiprilat decreased and AUC0-∞ increased obviously. It sug-gested that accumulation of ramiprilat occurred in body and the drug elimination became slower. No obvious difference of sunitinib pharmacokinetic behavior was found when it was given in combination with ramipril after a single-dose administration or multiple-dose administration. Sunitinib decreased the elimination of ramiprilat after co-administration in company with drug accumulation in body after multiple-dose co-administration. The study showed that there were pharmacokinetic interactions between sunitinib and ramipril in SD rats.

Objective To explore the role of insulin-like growth factor-2/insulin-like growth factor1 receptor/insulin receptor substrate-1 (IGF2/IGF1R/IRS1) signal pathway inducing the chemoresistance of epidermal growth factor receptor 2 (ErbB2) positive breast cancer cells to Herceptin.Methods Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot assay were used to determine the expression levels of IGF2,IGF1 R,and IRS1.The direct targets of miR-126 were validated by dual-luciferase reporter gene assay.In SKBR3/pool2 cells,IGF1 R activity was reduced by an inhibitor of IGF1 R,and IRS1 was knocked-down by shRNAs.Furthermore,3-(4,5-dimenthylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay was performed to evaluate the sensitivity of these treated cells to Herceptin.Results IGF2,IGF1 R,and IRS1 were significantly higher expressed in SKBR3/pool2 cell compared to that in SKBR3 cell.Western blot assay showed that IGF2/IGF1R/IRS1 was activated in SKBR3/pool2 cells.Bioinformatics analysis combined with luciferase activity suggested that miR-126 directly targeted IRS1.MTS results demonstrated that the chemosensitivity to Herceptin of SKBR3/ pool2 cells with inhibitor of IGF1R or shRNAs targeting IRS1 or overexpressing miR-126 was significantly reduced.Conclusions IGF2/IGF1R/IRS1 signal pathway confers to the chemoresistance of ErbB2 positive breast cancer cells to Herceptin.

[ ABSTRACT] AIM:To explore the expression pattern of microRNA-205 ( miR-205) in glioma tissues and its role in the invasion of glioma cells.METHODS:The expression of miR-205 and TBX18 was detected by real-time PCR and immunohistochemical observation, respectively.Transwell assay was used to examine the invasion change of U251 glioma cells after miR-205 overexpression via miR-205 mimics or decrease in miR-205 expression by miR-205 inhibitor.The target of miR-205 was searched by bioinformatics analysis combined with experimental analysis.The protein level of TBX18 was determined by Western blotting after siRNA transfection and Transwell assay was conducted.RESULTS:miR-205 expres-sion was downregulated in 82.6%of detected glioma tissues and TBX18 was significantly overexpressed in glioma tissues compared with normal tissues.miR-205 overexpression remarkably inhibited the invasion potential of U251 glioma cells with a decrease in the invasive cells (P<0.01), while inhibition of miR-205 significantly enhanced the invasion ability of U251 cells.Mechanically, miR-205 directly targeted TBX18 and downregulation of TBX18 also significantly inhibited the invasion potential of U251 cells with a decrease in the invasive cells ( P<0.01 ) .CONCLUSION: miR-205 expression is de-creased in glioma, and miR-205 inhibits glioma cell invasion via targeting TBX18.Our research contributes to the mecha-nisms responsible for glioma invasion and provides theoretical base for developing new therapeutic strategy to treat glioma.

] Objective To explore the role and mechanisms of FGF2 in chemo?resistance in breast cancer. Methods The inhibitors for different signal pathway were used to treat two drug?resistant breast cancer cell lines MCF?7/5?Fu and T47D/5?Fu established in our lab. MTS assay was used to determine chemo?sensitivity and Hoechst stain was used to measure apoptosis. Protein activation and FGF2 protein level in cell culture medium were detected by western blot and ELISA respectively. Results Akt inhibitor MK?2206 (20 nM) and mTOR inhibitor AZD8055 (2 nM) significantly reversed the chemo?resistance of MCF?7/5?Fu and T47D/5?Fu cell lines to 5?Fu and paclitaxel, but ERK1/2 inhibitor SCH772984 showed no significant effect. Compared to parent cell lines MCF?7 and T47D, p?Akt and p?S6K (represented as mTORactivity) levels were obviously up?regulated in MCF?7/5?Fu and T47D/5?Fu cell lines, and so do the FGF2 mRNA level and FGF2 protein level from culture medium. Moreover, FGFR inhibitor AZD4547 (4 nM) markedly reversed the chemo?resistance of MCF?7/5?Fu and T47D/5?Fu cell lines to 5?Fu and paclitaxel and down?regulated activation of FGFR?Akt?mTOR signal pathway. In agreement, FGF2 protein (10ng/ml) enhanced the chemo?resistance of MCF?7 and T47D cell lines to 5?Fu and paclitaxel and up?regulated activation of FGFR?Akt?mTOR signal pathway. Conclusion Activation of FGF2?FGFR?Akt?mTOR signal pathway promoted chemo?resistance of breast cancer cells.

Objective To evaluate the accuracy of auditory evoked potential index (AAI) in monitoring the depth of sevoflurane anesthesia in infants.Methods Fifty ASA Ⅰ or Ⅱ pediatric patients,aged 1-3 yr,scheduled for elective surgery under general anesthesia,were enrolled in this study.Anesthesia was induced with propofol,cisatracurium and remifentanil.The patients were tracheal intubated and mechanically ventilated.PET CO2 was maintained at 35-45 mm Hg.Anesthesia was maintained with inhalation of sevoflurane.Fresh gas flow was first set at 6 L/min for 15 min and then reduced to 3 L/min.The end-tidal sevoflurane concentration (CETSev) was maintained at 2.5%,2.8%,3.0%,3.5%,3.7% and 4.0%.Each CETSev was maintained for 3 min.AAI was continuously monitored before induction of anesthesia,after induction,immediately before sevoflurane inhalation,and at the 6 CET Sev.Results AAI was negatively correlated with CET Sev (r =-0.872,P ＜ 0.01).Conclusion AAI can accurately reflect the depth of sevoflurane anesthesia in infants.