Objective : To explore the effect of sericin on podocyte epithelial-mesenchymal transition induced by high glucose． Methods : Conditional immortalized mouse podocytes were used as the research object to construct podocyte injury model by high glucose stimulation．The podocytes were divided into normal (NG) group ，hyperton- ic control (MG) group ，high glucose injury ( HG) group ，low ，medium and high dose sericin ( LS ，MS ，HS) group．CCK-8 method was used to determine the viability of podocytes in each group ; the morphological structure of podocytes in each group was observed by ordinary optical inverted microscope．The migration ability was detected by Transwell and cell scratch test．Western blot was used to detect the expression levels of EMT-related mesenchy- mal phenotype factors Snai1，α-SMA，FSP-1，MMP-9 and epithelial phenotype factors Nephrin，E-cadherin，and WT-1 in podocytes of each group. Results : Compared with NG group，HG group showed lower podocyte activity (P＜0. 01) ，worse podocyte status and enhanced podocyte migration ability，up-regulated Snai1，α-SMA，FSP-1 and MMP-9 protein expressions (P ＜0. 01) ，and down-regulated Nephrin，E-cadherin and WT-1 protein expres- sions (P＜0. 01) ．Compared with HG group，the viability of podocytes in sericin group increased (P＜0. 05) ，the state of podocytes was improved ，the migration ability of podocytes was weakened ，the expression of Snai1 ，α - SMA，FSP-1 and MMP-9 was down-regulated (P＜0. 05) ，and the expression of Nephrin，E-cadherin and WT-1 was up-regulated (P ＜0. 05 ) ． Conclusion Sericin can alleviate podocyte epithelial-mesenchymal transition in- duced by high glucose.

Objective:To observe the effect of low-expression or over-expression of NUP88 gene on the proliferation and invasion ability of breast cancer cell line BT-20.Methods: NUP88 recombinant adenovirus expression vector and NUP88 RNAi adenovirus vector were transfected into breast cancer BT-20 cells to obtain BT-20 cells over-expressing NUP88 and BT-20 cells lower-expressing NUP88 and then detected the expression of NUP88 mRNA and NUP88 protein.After that,the apoptosis of BT-20 cells was detected by flow cytometry and the invasion and metastasis of BT-20 cells were detected by Transwell invasion assay.The expression of apoptosis protein and invasion and metastasis proteins were detected by Western blot.Results: BT-20 cell with the over expression levels of NUP88 mRNA and NUP88 protein and BT-20 cell with the low expression levels of NUP88 mRNA and NUP88 protein were structured.The over-expression of NUP88 gene led to proliferation rate and the number of invasive cells were significantly higher than BT-20 cells,apoptosis cells were significantly lower than BT-20 cells(P<0.05).However,the low-expression of NUP88 gene led to proliferation rate and the number of invasive cells were significantly lower than BT-20 cells,apoptosis cells was significantly higher than BT-20 cells(P<0.05).The over-expression of NUP88 gene led to Bcl-2 and β-catenin level were significantly higher than that of BT-20 cells,and Bax and E-cadherin level were significantly lower than that of BT-20 cells(P<0.05).However,the low-expression of NUP88 gene led to Bcl-2 and β-catenin level were significantly lower than that of BT-20 cells,and Bax and E-cadherin level were significantly higher than that of BT-20 cells(P<0.05).Conclusion: NUP88 gene regulates the proliferation and invasion and migration ability of breast cancer cells by regulating the expression of Bax,Bcl-2,E-cadherin and β-catenin.It has an important significance in the target treatment of breast cancer.