Single-crystal InAs nanowires (NWs) are synthesized using metal-organic chemical vapor deposition (MOCVD) and fabricated into NW field-effect transistors (NWFETs) on a SiO(2)/n(+)-Si substrate with a global n(+)-Si back-gate and sputtered SiO(x)/Au underlap top-gate. For top-gate NWFETs, we have developed a model that allows accurate estimation of characteristic NW parameters, including carrier field-effect mobility and carrier concentration by taking into account series and leakage resistances, interface state capacitance, and top-gate geometry. Both the back-gate and the top-gate NWFETs exhibit room-temperature field-effect mobility as high as 6580 cm(2) V(-1) s(-1), which is the lower-bound value without interface-capacitance correction, and is the highest mobility reported to date in any semiconductor NW.
Taken together, our results indicated that CD73 may facilitate the adhesion, migration and invasion of human breast cancer cells through its enzyme activity of generating adenosine. This study provided a possibly molecular mechanism of metastasis of breast carcinoma.
Ecto-5¢-nucleotidase (CD73), a cell surface protein that hydrolyzes extracellular AMP into adenosine and phosphate, is overexpressed in many solid tumors. In this study, we tested the hypothesis that increased CD73 may promote tumor progression by examining the effect of CD73 suppression via RNA interference and CD73 overexpression on tumor growth in vivo and in vitro. Using digitized whole-body images, plate clone forming assay and TUNEL assay in frozen tissue sections, we found that the cell growth rate was significantly lower in vivo and in vitro after CD73 suppression and late apoptosis was much higher in xenograft tumors developed from the CD73-siRNA transfected MB-MDA-231 clone (P1). By flow cytometry, the P1 cell cycle was arrested in the G0/G1 phase. Moreover, Bcl-2 was downregulated, while Bax and caspase-3 were upregulated with CD73 suppression. CD73 inhibitor a,b-methylene adenosine-5¢-disphosphate (APCP) functioned similarly with RNAimediated CD73 suppression. In addition, in transfected MCF-7 cells, we found that CD73 overexpression increased cell viability and promoted cell cycle progression, depending on its enzyme activity. More intriguingly, CD73 overexpression in MCF-7 breast cancer cells produces a tumorigenic phenotype. We conclude that CD73 plays an important role in breast cancer growth by affecting cell cycle progression and apoptosis. (Cancer Sci 2010; 101: 2561-2569 B reast cancer develops in 14% of women and is a leading cause of cancer death in women around the world.(1)Understanding the molecular mechanisms of breast carcinoma progression is important for effective treatments. Ecto-5¢-nucleotidase (CD73) is a 70 kDa glycosylated protein that is bound to the outer surface of the plasma membrane by a glycosyl phosphatidyl inositol anchor and co-localized with detergent-resistant and glycolipid-rich membrane sub-domains called lipid rafts.(2) CD73 hydrolyzes extracellular AMP into adenosine and phosphate. Adenosine, a proliferative factor, acting through Gprotein coupled receptors, produces a spectrum of physiological functions.(3) In addition, it causes tumor growth, angiogenesis and immune suppression.(4) CD73 upregulation is associated with a highly invasive cancer phenotype, drug resistance and tumor-promoting functions.(5) In addition to acting as a hydrolytic enzyme to generate adenosine, CD73 may serve as an adhesive molecule and interact with extracellular matrix glycoprotein, such as fibronectin and laminin, to produce cancer-invasive properties.(6) Bavaresco et al. (7) reported that CD73 mediated glioma cell proliferation depends upon adenosine. Furthermore, CD73 is overexpressed in the progression of many human solid tumors, such as breast cancer, (8,9) papillary thyroid carcinomas, (10) melanoma (11) and prostate cancer. (12) All these factors implicate the crucial role of CD73 in tumorigenesis. To date, our knowledge on the mechanisms of CD73 on tumor growth is still limited. Previously, we showed that CD73 may promote metastasis by facilitating the migration, adhesion and i...
Conductive atomic force microscopy has been used to characterize distance-dependent electron transport behavior in InAs nanowires grown by metal-organic chemical vapor deposition. Using a conducting diamond-coated tip as a local electrical probe in an atomic force microscope, the resistance of the InAs nanowire has been measured as a function of electron transport distance within the nanowire. Two regimes of transport behavior are observed: for distances of ϳ200 nm or less, resistance independent of electron transport distance, indicative of ballistic electron transport, is observed; for greater distances, the resistance is observed to increase linearly with distance, as expected for conventional drift transport. These observations are in very good qualitative accord with the Landauer formalism for mesoscopic carrier transport, and the resistance values derived from these measurements are in good quantitative agreement with carrier concentrations and mobilities determined in separate experiments. These results provide direct information concerning distances over which ballistic transport occurs in InAs nanowires as well as demonstrating the ability of the scanning probe techniques employed to characterize nanoscale transport characteristics in semiconductor nanowire structures.
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