PKC agonist PMA can regulate the expression of MMPs, TIMPs, uPA receptor, and uPA inhib itor PAI 1 The immunofluorescence results of this study showed that a 24 hour treatment with 100 nM stau rosporine resulted in 57. 39% and 48. 37% decreases in the level of MMP 9 and uPA respectively in A549 cells. This indicated selleckchem that staurosporine can decrease the invasive capability of cancer cells through the inhibition of MMP 9 and uPA protein levels in lung cancer cells and is con sistent with other reports We understand the importance of interpreting these Inhibitors,Modulators,Libraries results in the light of the increased apoptosis observed in staurosporine treated cells and the resulting loss in cell viability. Additionally, realizing that staurosporine is a non specific PKC inhibi tor, our future work will include assessing the role of more specific PKC inhibitors on cell adhesion and mobility in A549 cells.
Conclusion In summary, this study illustrates that staurosporine inhibits cell adhesion, mobility, and invasion of A549 cells. These effects could be mediated through the inhibi tion of PKC , induction of E Cad expression, and decreased integrin 1, LnR, MMP 9 and uPA levels. It is worth noting that staurosporine Inhibitors,Modulators,Libraries is a non specific PKC inhibitor with multiple biological effects. Therefore, addi tional studies are Inhibitors,Modulators,Libraries required to study the effect of stau rosporine in other cell lines. Our future goals include decoding the relationship between the various proteins tested herein and the staurosporine mediated decreases in adhesion, mobility, and invasiveness of A549 lung cancer cells.
Nevertheless, our results represent an important step forward in understanding Inhibitors,Modulators,Libraries the development of lung carci noma and designing novel strategies to inhibit metastasis of the tumor by targeting the adhesion, mobility and inva sive properties of these tumor cells. Background Breast cancer is the most common malignancy in women, accounting for 18% of all cancers, and is the leading cause of cancer deaths in women worldwide. Most of these deaths are due to metastatic disease. An increasingly accepted concept is that epithelial to mesenchymal transi tion, which is a normal developmental program, is an important preliminary Inhibitors,Modulators,Libraries step in metastasis. EMT involves a range of cellular phenotypic www.selleckchem.com/products/BI6727-Volasertib.html and func tional changes cell cell adhesion is disrupted and a more dynamic cell matrix adhesion is enhanced, polarity and cytoskeletal organization change, ECM molecule synthe sis and assembly are altered and an up regulation of the synthesis and activity of extracellular proteases occurs. An early central event in many EMTs is the downregula tion of the homophilic cell cell adhesion molecule E cad herin.
Related posts: