Background and purpose:About 80%patients with oral and maxillofacial malignant tumor are oral squamous cell carcinoma (OSCC). OSCC is one of the most common cancers in the world with less than 50%survival rate over 5 years. This experiment aimed to explore the effect of stanniocalcin 2 (STC2) on apoptosis, proliferation, migration and invasion of OSCC cell. Methods:RNA interference (RNAi) vector pLKO.1-shSTC2 was constructed and transfected into KB cells. Cell proliferation and cell apoptosis were then assessed by CCK8, APC Annexin V/7-AAD and lfow cytometry. Differences of migration and invasion between KB scr and KB STC2i were examined by cell scratch and transwell tests. Finally, this study detected the apoptosis-associated proteins and metastasis-associated proteins by Western blot. Results:STC2 down-regulation plasmid was constructed and transfected into KB cells. CCK8 prolifera-tion assay revealed that the STC2 down-regulation inhibited KB cells proliferation. By treating with cisplatin, this study found that STC2 silence could facilitate cell apoptosis signiifcantly. With the knock down of STC2 gene, the expressions of Bcl-2, Caveolin-1 andβ-catenin were decreased but the expression of bax was obviously increased. Conclusion:These data suggest that STC2 may be involved in the apoptosis, proliferation, migration and invasion of OSCC KB cells. Simultaneously, it can signiifcantly weaken the sensitivity of KB cells to chemotherapeutic drug cisplatin.

Recurrent laryngeal nerve palsy is one of the most serious complications associated with thyroid cancer surgery. This study aimed to assess the efficacy of intraoperative neural monitoring (IONM) in preventing recurrent laryngeal nerve palsy during thyroid cancer surgery, analyze and elaborate the theory, operation standard, application, benefits and disadvantage based on clinical practice.

The effects of adsorption time, solid-liquid ratio, sample concentration, flow rate on the adsorption properties of supported ionic liquids(the N-methylimidazolium functionalized silica, SilprMin) for flavonoids were investigated. The results indicated that the adsorption equilibrium for tested compounds, genistein, luteolin and quercetin, was achieved within 30 min, the adsorption efficiencies of these three compounds were improved with the increase of solid-liquid ratio, and decreased with the increase of their concentrations. Moreover, the adsorption isotherm data of the three tested compounds were in good concordance with the Langmuir model. The saturated adsorption capacity of SilprMim for genistein, luteolin and quercetin was 47.7, 52.5 and 63.2 mg/g, respectively. Adsorption efficiency of SilprMim could reach more than 90% at a sample flow rate of 0.5～1.5 mL/min. Using methanol as eluent, the saturated desorption efficiencies of genistein, luteolin and quercetin were 86.1%, 83.3% and 84.6%, respectively. The elution order of the three tested flavonoids was genistein, luteolin and quercetin. SilprMim had strong adsorption and separation capacity for three tested flavonoids, which was hopeful to be applied in separation and purification of naturally occurring flavonoids.

Objective: To study the effect of sulforaphane (SUL) on cell growth inhibition, cell cycle, apoptosis and its mechanism in different breast cancer cell lines. Methods: By means of MTT assay, flow cytometry and Western blotting, the effects of the SUL different concentrations on cell growth inhibition, cell cycle arrest, F3Ⅱapoptosis and expression of p34cdc2 and Cdc25C were studied. Results: (1) SUL had strong inhibition effects on the cell growth of tested mammary cancer cell lines, in which the sensitivity of ERP cell lines to SUL was stronger than that of ERN cell line. (2) SUL exhibited obviously G2/M cell cycle arrest to F3Ⅱ and two kinds of ERP cell lines at 5-10?mol/L, whereas no effect on the cell cycle of ERN cell line. (3)The mechanism of hindering transition of F3 Ⅱ cells from G2 phase to M phase was enhancing the phosphorylation of Cdc2, down-regulating the expression of Cdc25C, and inducing inhibition to thedephosphorylation of cyclin B1-Cdc2 complex. (4) No apoptosis was observed under tested conditions. Conclusion: Sulforaphane exhibited obvious differences in the inhibiting effects on the cell proliferation and cell cycle arrests of four different tested breast cancer cell lines, and did not induce apoptosis in F3Ⅱcell line under tested conditions. The mechanism of cell cycle arrest of F3Ⅱcell line appears to involve enhancing the phosphorylation of Cdc2, and down-regulating the expression of Cdc25C.

Objective To study the lab-scale simulated method of three-effect dynamic countercurrent extraction from Hedyotis diffusa by multi-index optimization and SPSS software.Methods Polyphenol content,flavonoids content,scavenging activity of samples on DPPH radicals,and extracting rate were considered as the optimization indexes.Orthogonal design method was used to optimize the four main factors of alcohol concentration,ratio of solid to solution,extracting temperature,and extracting times.Results The optimum condition is 70 min extraction time,solid to solution ratio of 1∶14,50% alcohol,extracting temperature 85 ℃.Conclusion The condition of large-scale industrialized production might be explored by studying the lab-scale simulated method of dynamic countercurrent extraction from H.diffusa.

Objective To explore the correlation between miR-25 and FBXO33 in renal cell carcinoma (RCC),and to analyze the relationship with apoptosis and prognosis of renal cell carcinoma.Methods The 511 RCC chip results,from 1998 to 2013,were downloaded from the Cancer Genome Atlas (TCGA)database,and were analyzed for the correlation between miR-25 and FBXO33 by Pearson test.The expression of fluorescein were detected with the FBXO33 3’UTR wild-type,mu-tant and blank control luciferase reporter gene treated by miR-25.The viability of cells transient translated by the miR-25 mimic,siRNA and the controls were detected by CCK8 method.The apoptosis of cells transient translated by the miR-25 mimic,siRNA and the controls were detected by flow cytometry.58 cases with follow-up data were screened from TCGA by expression of FBXO33 negative correlation miR-25.The survival was analyzed between low expression of miR-25 combined with FBXO33 high expression group (n=34)with high expression of miR-25 combined with FBXO33 low expression group (n=24),using Log-rank test and Gehan-Breslow-Wilcoxon test.Results FBXO33 was negatively correlated with miR-25 in RCC tissue (r=-0.161 1,Pearson test).Compared with the control group,miR-25 could reduce the RLU of wild type group to 80.2%±2.6%,the difference was statistically significant (t=6.539,P=0.006).The RLU of mutation group was 103.5%±8.4% compared with that of blank control group,the difference was not statistically significant (t=0.041 3,P=0.968 4),compared with the blank group in 72h for the cell varibility,miR-25 siRNA group were elevated by 32.7%± 3.5%,the difference was statistically significant (P<0.05).The miR-25 mimic group were reduced by 23.3%±1.7%,the difference was statistically significant (P<0.05),and compared with the control group,the early apoptosis rate was de-creased in mimic-miR-25-3p group (8.83 ± 0.09 vs 12.83 ± 0.14),while the difference was statistically significant (t=42.17,P=0.005).The late apoptosis rate was slightly escalated (0.41±0.10 vs 0.33±0.15),while the difference was not statistically significant (t=0.75,P=0.639).Compared with the control group,the early apoptosis rate was increased in siR-NA-miR-25-3p group (19.05 ± 1.64 vs 13.68 ± 0.78),while the difference was statistically significant (t=5.12,P=0.006).But the late apoptosis rate was reduced (0.56±0.10 vs 0.62±0.08),while the difference was not statistically sig-nificant (t=0.83,P=0.376).The survival rate was higher in patients with low expression of miR-25 combined with high expression of FBXO33 (n=34)than that of miR-25 high expression combined with low expression of FBXO33 (n=24),the difference was statistically significant (Log-rank test P=0.025 2,Gehan-Breslow-Wilcoxon test P=0.004 9).Conclusion MiR-25 can inhibite FBXO33 in renal cell carcinoma,improve the cell activity,inhibit apoptosis and reduce the prognosis.

Stanniocalcin (STC) was ifrst found as a calcium- and phosphate-regulating hormone produced in bony ifsh by the corpuscles of Stannius. In mammals, the homolog STC-1 displays a relative high amino acid sequence identity (nearly 50%) with ifsh STC, and STC-2 has a lower identity (nearly 35%) with STC-1 and ifsh STC. Both STC-1 and STC-2 are expressed in a variety of tissues. The functions of STC have not been understood. But some ifndings have been reported on their cellular localization, gene structure, and expression in different physiological and pathological conditions, which will be clues in elucidating the functions of STC in mammals. Moreover, STC-1 and STC-2 are expressed in many tumor cell lines, suggesting other biological functions of STC in mammals other than mineral metabolism.

To study the mechanisms whereby cisplatin suppresses survival of human esophageal squamous cell carcinoma cells.The cytotoxicity of cisplatin in cisplatin-resistant cell line EC109 /CDDP and its parental cell line EC109 was measured by cell viability assay.Western blotting was used to investigate the protein expression of to-tal p53 and phosphorylated p53 at Ser15.Colony formation assay was employed to evaluate the ability of cells to recover from treatments and form colonies.The results indicated that EC109 /CDDP cells were more resistant to cisplatin-induced cytotoxicity than EC109 cells,with the IC50 values of (20.4 ±4.4)μmol /L and (5.7 ±0.1 )μmol /L,respectively.Although cisplatin did not alter the total protein level of p53,it obviously increased the phosphorylation of p53 at Ser15.Cisplatin inhibited survival of both EC109 /CDDP and EC109.Notably,inhibition of p53 by Pifithrin-αsignificantly promoted recovery of cisplatin-treated EC109 and EC109 /CDDP cells to differ-ent degrees.In this respect,p53 protein was found to be activated in response to cisplatin treatment in both EC109 /CDDP and EC109,which may contribute to the cytotoxic effect of cisplatin.