CD82 Suppresses ADAM17-Dependent E-Cadherin Cleavage and Cell Migration in Prostate Cancer.

CD82 acts as a tumor suppressor in a series of steps in malignant progression. Here, we identified a novel function of CD82 on posttranslational regulating E-cadherin in prostate cancer. In our study, the declined expression of CD82 was verified in prostate cancer tissues and cell lines compared with normal tissue and cell lines. Functionally, CD82 inhibited cell migration and E-cadherin cleavage from the cell membrane in prostate cancer cell. Further study proved that a disintegrin and metalloproteinase ADAM17 as an executor of E-cadherin cleavage mediated the inhibitory regulation of CD82 in E-cadherin shedding in prostate cancer. Specifically, CD82 interacted with ADAM17 and inhibited its metalloprotease activity, which led to the descent of E-cadherin shedding. These results show a nuanced but important role of CD82 in nontranscriptional regulation of E-cadherin, which may help to understand the intricate regulation of dysfunctional adhesion molecule in cancer progression.

Removal of NO with the hexamminecobalt solution catalyzed by the carbon treated with oxalic acid.

NO can be removed at the same time with SO2 by aqueous Co(NH3)62+ solution. The reduction of Co(NH3)63+ to Co(NH3)62+ is catalyzed by activated carbon to regain the NO absorption ability of the scrubbing solution. Oxalic acid solution is explored to change the carbon surface to ameliorate its catalytic capability. The experimental results suggest that the best catalyst is prepared by impregnating the carbon sample in 0.7 mol l-1 oxalic acid solution for 24 h followed by being activated at 600 °C for 5 h under nitrogen atmosphere. After being treated with oxalic acid solution, the surface area and the acidity on the carbon surface increase. The experiments show that the carbon modified with oxalic acid can get a much higher NO removal efficiency than the original carbon.