AIM To find a new method for purifying the active compound 5F isolated from Pteris semipinnata L.(PsL ) and observe its enhanced cytotoxicity when combined with other antitumor agents. METHODS Silica gel combined with AgNO 3 was made to purify 5F. Cytotoxicity was detected with trypan blue dye exclusion assay. RESULTS After purification, the concentration of compound 5F in purified products was higher than 99%. The inhibitory rates of 5F combined with 5 Fu or CDDP or VCR were higher than that of these drugs used alone. CONCLUSIONS Compound 5F could be purified effectively using silica gel combined with AgNO 3. 5F could enhance the cytotoxicity on HL 60 and K562 cells of the drugs mentioned above. The different effect of these agents on the various phases of cell cycle kinetics may explain the enhanced effect of 5F.

Object To prepare the water soluble quercetin arginine complex (QAC) and widen the administration path of quercetin (QUE). Methods Definite QUE and L arginine were refluxed in alcohol to prepare QAC. The QAC structure was identified by micellar paper chromatography, UV spectrometry, IR spectrometry, and X ray diffraction. Results QAC was prepared from QUE and L arginine in molar ratio 1∶1. The inhibitory activity of QAC that existed stably in room temperature on cancer cell growth was as strong as that of QUE, and the solubility of QAC in water was remarkably enhanced. Conclusion The above preparation method is simple and available, and it is suitable to improve the bioavailability.

Objective We investigated the expression profile of cancer related genes in hMSCs co-cultured with U251 glioma cells, to evaluate the risk of malignant transformation of hMSCs in glioma environment. Methods hMSCs were co-cultured with U251 glioma cells for 5 days and the expression profile of cancer-related genes were investigated by using microarray assay, followed by Real-time quantitative RT-PCR and Western blot. Results Of the 440 cancer-re?lated genes covered by Oligo GEArray Human Cancer Microarray OHS-802, SPINT2, TK1, STC1, MMP1, CCND1, SORT1, SEPT6, CDC20, SHB, CDK5, RELA, XRCC4, KIT, CTPS, CAPNS1 and ETV6 were significantly upregulated (>3-fold) whereas none was downregulated in hMSCs co-cultured with U251 glioma cells. The upregulation of oncogenes KIT, CAPNS1, TK1, MMP1, CCND1, CDC20, RELA and STC1 in co-cultured hMSCs were confirmed by Real-time quan? titative RT-PCR. The upregulation of protein expression of oncogenes KIT, MMP1, CCND1 and RELA were detected by Western blot. Conclusion The present study demonstrates that co-culture of hMSCs with human glioma cells leads to up?regulation of some important oncogenes in hMSCs, indicating the tumorigenic potential of hMSCs in glioma environment.

Objective To investigate the effects of saturated fatty acids and unsaturated fatty acids on proliferation and autophagy of human lung cancer cells. Methods The lung cancer cells A549 were treated with stearic acid (saturated fatty acid) and doconexent (DHA, unsaturated fatty acid), respectively, in concentrations of 0, 30, 60, 120 and 240μmol/L. MTT test and cell clone formation assay were performed to detect the proliferation of A549 cells. The morphology of A549 autophagy was observed by confocal laser scanning microscopy after A549 cells were treated with stearic acid or DHA for 24 hours. Western blotting assay was used to detect the expression of autophagy-related protein after A549 cells were treated with stearic acid or DHA for 12, 24 and 36 hours, respectively. Results 30-240μmol/L stearic acid or DHA both inhibited the proliferation of A549 cells (P<0.05). Both stearic acid and DHA induced autophagy of A549 cells, meanwhile, down-regulated Phospho-mTOR (ser2481) and up-regulated LC3Ⅱ/LC3Ⅰ of A549 cells (P<0.05). Conclusions Both saturated fatty acid and unsaturated fatty acid can inhibit the proliferation and induce autophagy of lung cancer cells. The mechanisms of autophagy may be related to Phospho-mTOR (ser2481) signaling pathway.