Regarding radioactive iodine-refractory failure or advanced differentiated thyroid cancer,multiple multikinase inhibitors including sorafenib and lenvatinib,which target platelet derived growth factor receptor,vascular endothelial growth factor pathway,and rearranged during transfection (RET) pathway were proved to have obvious antitumor activity.Moreover,selective BRAF inhibitor,promoting drug uptake of radioactive iodine also showed a certain therapeutic effect.These molecular targets which are relevant with differentiated thyroid cancer occurrence,development,invasion and metastasis have become of its moment,and,selective inhibitors and re-differentiation agents were shown to be promising.In the future,individual genetic testing would provide more specific information in directing individualized molecular-targeted therapy.

Objective To explore the role of the SerpinB5 and β-catenin in occurrence and development of the primary hepatocellular carcinoma (HCC). Methods The expressions of SerpinB5 and β-catenin protein and mRNA in carcinoma tissues and paracancerous tissues of 60 patients with primary HCC were detected by immumohistochemistry and real-time quantitative reverse transcriptional polymerase chain reaction (RT-PCR) methods. Results The positive expression rate of SerpinB5 protein and SerpinB5 mRNA in carcinoma tissues were significantly lower than those in paracancerous tissues:25.0%(15/60) vs. 63.3%(38/60) and 1.12 ± 0.43 vs. 5.19 ± 0.39, and there were statistical differences (P<0.01). The positive expression rate of β-catenin protein and β-catenin mRNA in carcinoma tissues were significantly higher than those that in paracancerous tissues: 65.0%(39/60) vs. 31.7%(19/60) and 4.23 ± 0.25 vs. 1.19 ± 0.17, and there was statistical difference (P<0.01). Decreased SerpinB5 expression was associated with higher serumα-fetoprotein level, larger tumor size, poor differentiation, advanced TNM stage, capsule invasion and tumor thrombosis (P < 0.01 or 0.05). Increased β-catenin expression was associated with poor differentiation, advanced TNM stage, capsule invasion and tumor thrombosis (P < 0.01 or < 0.05). The correlation analysis result showed that SerpinB5 had negative correlation withβ-catenin (carcinoma issues:r=-0.346, P=0.001;paracancerous tissues:r=-0.258, P = 0.024). Conclusions The abnormal expression of SerpinB5 and β-catenin may contribute to the progression and biologically malignant behavior of primary HCC, and SerpinB5 and β-catenin exists synergistic effect in the occurrence and development of primary HCC.

ABSTRACT:Objective To investigate the effects of total flavones of oldenlandia diffusa (FOD)on epithelial-mesenchymal transition in hepatocellular cancer cell line MHCC97-H.Methods TGF-β1 induced EMT in routinely cultured liver cancer cell line MHCC97-H;then MHCC97-H cell was divided into 5 groups:normal control group, TGF-β1 group,TGF-β1 + FOD group,TGF-β1 + 5-FU group,and TGF-β1 + FOD + 5-FU group.After 48 h of treatment,the invasion ability of MHCC97-H cell was detected by Transwell;the proteins of E-cadherin and vimentin were determined by Western blot.Results Compared with the normal form of MHCC97-H cell line,the cell had obvious long fusiform after TGF-β1 induction,and the invasion ability enhanced (P = 0.02 ).But after treatment,the invasion ability of MHCC97-H cell decreased in FOD group and 5-FU group compared with that in TGF-β1 group (P = 0.03,P = 0.02 ),and decreased more significantly in FOD + 5-FU group (P = 0.01 ).The expression of E-cadherin at the protein level decreased significantly (P = 0.01 )in TGF-β1 group,which was abolished in FOD group (P =0.03 )and 5-FU group (P = 0.02 ).The expression of vimentin at the protein level increased significantly (P =0.01)in TGF-β1 group,which was abolished in FOD group (P =0.04)and 5-FU group (P =0.03)and more obviously in FOD+5-FU group (P =0.01).Conclusion FOD can reverse the invasion of MHCC97-H cells in EMT induced by TGF-β1 through decreasing the expression of E-cadherin protein and inhibiting the epithelial-mesenchymal transition of MHCC97-H cell.

Objective:To investigate the differences in the expression of microRNA (miR)-216a and its target gene SerpinB5 at the tissue level, and the effects of miR-216a on the proliferation of different liver cancer cells by regulating the expression of SerpinB5.Methods:Through bioinformatics prediction and selection of miR-216a that regulated SerpinB5. the expressions in liver cancer and normal tissues were detected by real time polymerase chain reaction (PCR). The miR-216a simulacrum and inhibitor, si-Serpinb5 and pcdna3.1-Serpinb5 to HepG2 and MHCC97H (97H) were transfected with liposomes, respectively. Real time PCR and Wester-Blot were used to detect the expression of miR-216a and SerpinB5 before and after transfection, and CCK8 was used to detect the influence of both on the proliferation of liver cancer cells.Results:The expression of miR-216a in human liver cancer tissues was higher than that in adjacent tissues, and the difference was statistically significant ( P < 0.01). The expression of SerpinB5 in human liver cancer tissues was lower than that adjacent tissues, and the difference was statistically significant ( P < 0.01). In HepG2 and 97H, miR-216a inhibitor and SerpinB5 overexpression group showed down-regulated miR-216a expression, which was statistically different from the control group ( P < 0.01). The proliferation of miR-216a inhibitor and pcdna3.1-serpinb5 group was lower than the control group, with statistically significant differences ( P < 0.01). Conclusions:The high expression of SerpinB5 can inhibit the proliferation of liver cancer cells, suggesting that SerpinB5 may have an anti-oncogene effect. MiR-216a may negatively regulate the expression of SerpinB5 and affect the proliferation of HCC cells.