RNAi-mediated silencing of CD147 inhibits tumor cell proliferation, invasion and increases chemosensitivity to cisplatin in SGC7901 cells in vitro

<p>Abstract</p> <p>Background</p> <p>CD147 is a widely distributed cell surface glycoprotein that belongs to the Ig superfamily. CD147 has been implicated in numerous physiological and pathological activities. Enriched on the surface of many tumor cells, CD147 promotes tumor growth, invasion, metastasis and angiogenesis and confers resistance to some chemotherapeutic drugs. In this study, we investigated the possible role of CD147 in the progression of gastric cancer.</p> <p>Methods</p> <p>Short hairpin RNA (shRNA) expressing vectors targeting CD147 were constructed and transfected into human gastric cancer cells SGC7901 and CD147 expression was monitored by quantitative realtime RT-PCR and Western blot. Cell proliferation, the activities of MMP-2 and MMP-9, the invasive potential and chemosensitivity to cisplatin of SGC7901 cells were determined by MTT, gelatin zymography, Transwell invasion assay and MTT, respectively.</p> <p>Results</p> <p>Down-regulation of CD147 by RNAi approach led to decreased cell proliferation, MMP-2 and MMP-9 activities and invasive potential of SGC7901 cells as well as increased chemosensitivity to cisplatin.</p> <p>Conclusion</p> <p>CD147 involves in proliferation, invasion and chemosensitivity of human gastric cancer cell line SGC7901, indicating that CD147 may be a promising therapeutic target for gastric cancer.</p

Size and promoter effects on iron nanoparticles confined in carbon nanotubes and their catalytic performance in light olefin synthesis from syngas

International audienc

Size and promoter effects on iron nanoparticles confined in carbon nanotubes and their catalytic performance in light olefin synthesis from syngas

International audienc

Synergy of nanoconfinement and promotion in the design of efficient supported iron catalysts for direct olefin synthesis from syngas

International audienc

Synergy of nanoconfinement and promotion in the design of efficient supported iron catalysts for direct olefin synthesis from syngas

International audienc

Additional file 2 of An integrated microfluidics platform with high-throughput single-cell cloning array and concentration gradient generator for efficient cancer drug effect screening

Additional file 2: Table S1. Acute myeloid leukemia patients’ characteristics

Additional file 1 of An integrated microfluidics platform with high-throughput single-cell cloning array and concentration gradient generator for efficient cancer drug effect screening

Additional file 1: Fig. S1. Design and simulation of the microfluidic device. Fig. S2. Overall pattern of the fabricated microfluidic device (a) and fabricated microchamber array (b). Fig. S3. Single cell array formed in the single-plexed device and the single-cell derived clones in a typical experiment. Fig. S4. Evaluation of on-chip cell proliferation. Fig. S5. Characterization of the on-chip concentration gradient generation. Fig. S6. Images of the single K562 cell array after the treatment of Imatinib (a) or Resveratrol (b) for 24 h on the microfluidic device. Fig. S7. Single drug treatment (Imatinib) of single K562 cell derived clones. Fig. S8. Single drug treatment (Resveratrol) to single K562 cell derived clones. Fig. S9. Separation of CD34+ acute myeloid leukemia cells from patient bone marrow species. Fig. S10. Optimized microchamber array for primary cell capture. Fig. S11. Evaluation of the concentration gradient generation on the modified device with fluorescein sodium (green) and sulforhodamine B (red) under 0.05 μl/min

Increased endoplasmic reticulum stress response is involved in clopidogrel-induced apoptosis of gastric epithelial cells.

The widespread use of clopidogrel alone or in combination with aspirin may result in gastrointestinal mucosal injury, clinically represented as recurrent ulceration and bleeding complications. Our recent work suggested that clopidogrel significantly induced human gastric epithelial cell (GES-1) apoptosis and disrupted gastric mucosal barrier, and that a p38 MAPK inhibitor could attenuate such injury. However, their exact mechanisms are largely unknown.The GES-1 cells were used as a model system, the effects of clopidogrel on the whole gene expression profile were evaluated by human gene expression microarray and gene ontology analysis, changes of the mRNA and protein expression were determined by real-time PCR and Western blot analysis, and cell viability and apoptosis were measured by MTT assay and flow cytometry analysis, respectively.Gene microarray analysis identified 79 genes that were differentially expressed (P<0.05 and fold-change >3) when cells were treated with or without clopidogrel. Gene ontology analysis revealed that response to stress and cell apoptosis dysfunction were ranked in the top 10 cellular events being affected, and that the major components of endoplasmic reticulum stress-mediated apoptosis pathway - CHOP and TRIB3- were up-regulated in a concentration- and time-dependent manner when cells were treated with clopidogrel. Pathway analysis demonstrated that multiple MAPK kinases were phosphorylated in clopidogrel-treated GES-1 cells, but that only SB-203580 (a p38-specific MAPK inhibitor) attenuated cell apoptosis and CHOP over-expression, both of which were induced by clopidogrel.Increased endoplasmic reticulum stress response is involved in clopidogrel-induced gastric mucosal injury, acting through p38 MAPK activation

Gene therapy for colorectal cancer by an oncolytic adenovirus that targets loss of the insulin-like growth factor 2 imprinting system

Abstract Background Colorectal cancer is one of the most common malignant tumors worldwide. Loss of imprinting (LOI) of the insulin-like growth factor 2 (IGF2) gene is an epigenetic abnormality observed in human colorectal neoplasms. Our aim was to investigate the feasibility of using the IGF2 imprinting system for targeted gene therapy of colorectal cancer. Results We constructed a novel oncolytic adenovirus, Ad315-E1A, and a replication-deficient recombinant adenovirus, Ad315-EGFP, driven by the IGF2 imprinting system by inserting the H19 promoter, CCCTC binding factor, enhancer, human adenovirus early region 1A (E1A) and enhanced green fluorescent protein (EGFP) reporter gene into a pDC-315 shuttle plasmid. Cell lines with IGF2 LOI (HCT-8 and HT-29), which were infected with Ad315-EGFP, produced EGFP. However, no EGFP was produced in cell lines with maintenance of imprinting (HCT116 and GES-1). We found that Ad315-E1A significantly decreased cell viability and induced apoptosis only in LOI cell lines in vitro. In addition, mice bearing HCT-8-xenografted tumors, which received intratumoral administration of the oncolytic adenovirus, showed significantly reduced tumor growth and enhanced survival. Conclusions Our recombinant oncolytic virus targeting the IGF2 LOI system inhibits LOI cell growth in vitro and in vivo, and provides a novel approach for targeted gene therapy.</p