Effect of 3,3′-Biisofraxidin on Apoptosis of Human Gastric Cancer BGC-823 Cells

Purpose: To study the effect of 3,3′-biisofraxidin from Sarcandrae Herba on the proliferation of BGC- 823 cells and the possible mechanisms.Methods: Cell Counting Kit-8 (CCK-8), flow cytometry, Western blot and xenograft assays were used to determine the effects of 3,3′-biisofraxidin on the proliferation, apoptosis, apoptotic proteins and xenograft of BGC-823 cells.Results: 3,3′-Biisofraxidin significantly (p < 0.01) inhibited the proliferation of BGC-823 cells (concentrations: 10 - 40 μM; cell viability: 30.45 - 76.68 % in CCK-8 assay) with half maximal inhibitory concentration (IC50) value of 20.35 μM and induced the apoptosis of BGC-823 cells (concentrations: 10, 20 and 40 μM; apoptotic cells: 11.92, 20.10 and 33.64 % in flow cytometry assay), compared with the control (cell viability: 99.73 %; apoptotic cells: 5.18 %). 3,3′-Biisofraxidin (10, 20 and 40 μM in vitro; 40 mg/kg in vivo) significantly (p < 0.05 or 0.01) down-regulated the expressions of anti-apoptotic proteins (Bcl-2, Bcl-xl and Survivin) and up-regulated the expressions of pro-apoptotic proteins (Smac, caspase-3, caspase-7 and caspase-9), compared with the control. Moreover, the release of cytochrome c from the mitochondria to the cytoplasm was significantly (p < 0.01) promoted in vitro, compared with the control. 3,3′-Biisofraxidin (40 mg/kg) significantly (p < 0.05 or 0.01) inhibited the growth of tumor in xenograft assay, compared with the control.Conclusion: 3,3′-Biisofraxidin significantly induces the apoptosis of BGC-823 cells in vitro and in vivo through the mitochondria-mediated apoptotic pathway, and therefore has a potential to be developed into an anti-gastric cancer drug.Keywords: Sarcandrae Herba, Gastric cancer, 3,3′-Biisofraxidin, Mitochondria-mediated apoptotsis, Cell Counting Kit-8, Xenograf

Proteome analysis of human colorectal cancer tissue using 2-D DIGE and tandem mass spectrometry for identification of disease-related proteins

Laser capture microdissection and two-dimensional difference gel electrophoresis were used to establish the proteomic profiles for tumor and matched adjacent tissues from 12 patients. Differential protein spots were identified by mass spectrometric analysis. The cDNA of the differential protein was transfected into colorectal cancer cells, and the biological behavior of these cells was observed. The proteomic profile in colorectal cancer tissues was significantly different from that in normal adjacent tissues. There was a 1.5-fold difference and 60 differential protein spots between cancer and adjacent tissues. Ten differential protein spots were analyzed. Among them, two protein spots were down-regulated and eight protein spots were up-regulated in the primary tumor tissues. After identification by mass spectrometry, the two down-regulated proteins were carbonic anhydrase II and protein disulfide isomerase, and these eight up-regulated proteins included APC-stimulated guanine nucleotide exchange factor, phosphoglycerate kinase 1, fumarate hydratase, aldolase A, activator protein 2B, glutathione S-transferase A3, Arginase and zinc finger protein 64 homolog. After been transfected with carbonic anhydrase II, the invasive ability, mobility and drug resistance of colon cancer lovo cells were significantly reduced. The proteomic profile was significantly different between colorectal cancer tissues and normal adjacent tissues. The down-regulation of carbonic anhydrase II and protein disulfide isomerase and up-regulation of APC-stimulated guanine nucleotide exchange facto, aldolase A, glutathione S-transferase A3 and arginase were correlated with the onset of colorectal cancer.Key words: Colorectal cancer, proteomics

Layer-dependent transport properties in the Moir\'e of strained homobilayer transition metal dichalcogenides

Bilayer moir\'e structures have attracted significant attention recently due to their spatially modulated layer degrees of freedom. However, the layer-dependent transport mechanism in the moir\'e structures is still a problem to be explored. Here we investigate the layer-dependent transport properties regulated by the strain, the interlayer bias and the number of moir\'e periods in a strained moir\'e homobilayer TMDs nanoribbon based on low-energy efficient models. The charge carriers can pass perfectly through the scattering region with the moir\'e potential. While, it is noted that the overall transmission coefficient is mainly contributed from either intralayer or interlayer transmissions. The transition of transport mechanism between intralayer and interlayer transmissions can be achieved by adjusting the strain. The intralayer transmissions are suppressed and one of the interlayer transmissions can be selected by a vertical external electric field, which can cause a controllable layer polarization. Moreover, the staggered intralayer and interlayer minigaps are formed as the number of moir\'e periods increases in the scattering region due to the overlap of the wave functions in two adjacent moir\'e periods. Our finding points to an opportunity to realize layer functionalities by the strain and electric field.Comment: 6 pages, 4 figure