Traditional treatments for malignant tumor are far from meeting the clinical demands.Recently,research on anti-tumor targeted drugs has made a significant breakthrough,which brings new hope for the treatment of malignant tumor.Anti-tumor targe-ted drugs can specifically target malignant tumor and directly in-hibit the growth of tumor cells,showing no toxicity to the normal tissues and organs.Herein we reviewed the research progress of small molecular targeted drugs and antibody targeting new drugs.

Objective: To study the hypoglycemic effects of soybean isoflavones (SI) and soyasaponins (SS) in diabetes, and their inhibitory activities on alpha-glucosidase (EC 3.2.1.20) and alpha-amylase (EC 3.2.1.1). Methods: GK/Jcl type 2 diabetic rats were given diet containing 20 g/kg of soybean hypocotyl extracts (SHE) for 20 weeks, then the blood glucose and oral glucose tolerance test were observed. SI and SS were isolated by ODS column chromatography and high-performance liquid chromatography (HPLC) from SHE. The inhibitory activities of each component of SI and SS against alpha-glucosidase and alpha-amylase were tested by colorimetric method. Results: SHE decreased blood glucose significantly in type 2 diabetic rats and improved glucose tolerance in both normal and diabetic rats. In alpha-glucosidase inhibitory assay, Group B, Group E and DDMP (2,3-dihydro-2,5-dihydroxy-6-methyl-4H-pyran-4-one) saponins showed potent inhibitory activities with IC50 values of 10-40 靘ol/L. Isoflavone aglycones also showed potent inhibitory activities against alpha-glucosidase with IC50 values of 20-150 mol/L, while isoflavone glycosides showed a little lower potencies. Inhibition of SI and SS on alpha-amylase was low, and their inhibitory activities were about 10%~20% at the concentration of 1g/L. Conclusion: SI and SS may decrease blood glucose and improve oral glucose tolerance in diabetic rats, probably via the inhibitory effects on alpha-glucosidase and alpha-amylase.

ObjectiveTo investigate the effect of iridoid glycosides from Boschniakia rossica （IGBR） on epithelial-mesenchymal transition （EMT） of HepG2 hepatoma cells induced by transforming growth factor-beta 1 （TGF-β1）. MethodsHepG2 hepatoma cells were induced by 10 μg/L TGF-β1 to construct an EMT model of hepatoma cells. The cells were divided into control group （treated with serum-free DMEM）， model group （treated with 10 μg/L TGF-β1）， and IGBR group （treated with 10 μg/L TGF-β1 and 500 mg/L IGBR）， and all cells were cultured for 48 hours. Cell adhesion assay， wound healing assay， and Transwell chamber assay were used to observe the migration and invasion abilities of cells. RT-PCR and Western blot were used to measure the mRNA and protein expression levels of E-cadherin， N-cadherin， and vimentin in cells， and Western blot was used to measure the protein expression levels of Slug， Twist1， ZEB1， p-STAT3， and STAT3. A one-way analysis of variance was used for comparison of continuous data between multiple groups， and the least significant difference t-test was used for further comparison between two groups； the independent-samples t test was used for comparison between two groups. ResultsAfter TGF-β1 induction， HepG2 cells in the model group showed long spindle-shape changes， while those in the control group showed polygonal epithelia-like changes. Compared with the model group， the IGBR group had a significant reduction in cell adhesion rate and significant inhibition of cell migration and invasion abilities （all P<0.05）， as well as significant increases in the mRNA and protein expression levels of E-cadherin （P<0.05）， significant reductions in the mRNA and protein expression levels of N-cadherin and vimentin （all P<0.05）， and significant reductions in the protein expression levels of Slug， Twist1， ZEB1， and p-STAT3 （all P<0.05）. ConclusionIGBR can inhibit TGF-β1-induced EMT process in HepG2 cells， thereby attenuating cell adhesion， migration， and invasion abilities， and it can also upregulate E-cadherin， downregulate N-cadherin and vimentin， and upregulate the protein expression of Slug， Twist1， ZEB1， and STAT3， possibly by inhibiting the STAT3 pathway to downregulate the EMT transcription factors such as Slug， Twist1， and ZEB1.