Liu Xinghan

Bmf is upregulated by PS-341-mediated cell death of glioma cells through JNK phosphorylation.

Malignant glioma is resistant to the induction of apoptosis, resulting in a subsequent failure of chemotherapy in clinical treatment strategies. Downregulation of bcl-2 and bcl-xl expression in glioblastoma cells can induce apoptosis. BH3-only proteins, which include Bmf, are essential initiators of stress-induced cell death and apoptosis. Whether PS-341 regulates expression of BH3-only proteins in glioblastoma cells during the procedure of apoptosis is unclear. This study was designed to investigate the effects of PS-341 on glioma cell death and its possible signaling pathway. Our results demonstrate that Bmf is upregulated by PS-341 in A172 and T98G cells, and Bmf has a crucial role in PS-341-mediated cell death. In addition, we found that expression of Bmf is regulated by JNK phosphorylation.

The Effect of Tumstatin Anti-tumor Peptide on Proliferation and Apoptosis of Different Cells

Tumstatin anti-tumor peptide of 19peptide can inhibit the proliferation of melanoma tumor cell. To study its effect on the proliferation and apoptosis of different cells and verify its no anti-tumor specificity, the base sequence of 19peptide was designed and constructed engineering bacteria. The soluble 19peptide was obtained from one step chitin affinity chromatograph. By such experiment as MTT assay, cell growth curve, TUNEL assay, flow cytometry, chick chorioallantoic membrane (CAM),transmission electron microscopy(TEM), the tumor inhibition experiment of mice ascitic fluid transfevent H22 hepatoma, the biological activity of 19peptide was studied. Experiments in vitro and in vivo identified that obtained 19peptide could inhibit proliferation of hela cell and promote its apoptosis. It also could affect proliferation of endothelial cell to some extent. Its anti-tumor effect will lay foundation on its mechanism of action research and clinically tumor therapy in future.

Cloning and biological activity of an anti-tumor peptide of Tumstatin

To obtain an anti-tumor peptide of Tumstatin and detect its biological activity, the nucleotide sequence encoding 185–203 amino acids (19peptide) of Tumstatin was synthesized and inserted into the fusion protein vector pTYB2. After identification by sequencing and restriction endonucleases, the recombined vector was transformed into BL-21 (DE3) E. coli competent cells. Transformed E. coli BL-21 (DE3) were induced by isopropyl-β-thiogalactopyranoside (IPTG), and then expressed. By 1,4-dithiothreitol (DTT) reduction, the soluble 19peptide was obtained from a chitin affinity chromatograph. The biological activity of 19peptide was determined by 3-[4,5-dimethylthiazol-2-y1]-2,5-diphenytetrazolium bromide (MTT) assay, cell growth curve, the effect of the ascitic fluid transfevent H22 hepatoma on mice and via histopathological slices. The purified 19peptide directly inhibited proliferation and migration of murine B16 melanoma cells, SMMC-7721hepatoma carcinoma cells and human umbilical vein endothelial cells (HUVEC). The tumor inhibition rate of mice ascitic fluid transfevent H22 hepatoma was 48.46%. Histopathological slices showed that it could promote tumor tissue necrosis and decrease the density of blood vessels. With higher anti-tumor activity, 19peptide has the potential to become a novel, potent anti-tumor agent.