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Articles by C. W Nam
Total Records ( 2 ) for C. W Nam
  Y. M Yang , S Lee , C. W Nam , J. H Ha , M Jayaraman , D. N Dhanasekaran , C. H Lee , M. K Kwak and S. G. Kim
 

Bortezomib is a proteasome inhibitor approved for anticancer therapy. However, variable sensitivity of tumor cells exists in this therapy probably due to differences in the expression of proteasome subunits. G12/13 serves modulators or signal transducers in diverse pathways. This study investigated whether cancer cells display differential sensitivity to bortezomib with reference to G12/13 expression, and if so, whether G12/13 affects the expression of proteasome subunits and their activities. Bortezomib treatment exhibited greater sensitivities in Huh7 and SNU886 cells (epithelial type) than SK-Hep1 and SNU449 cells (mesenchymal type) that exhibited higher levels of G12/13. Overexpression of an active mutant of G12 (G12QL) or G13 (G13QL) diminished the ability of bortezomib to induce cytotoxicity in Huh7 cells. Moreover, transfection with the minigene that disturbs G protein-coupled receptor-G protein coupling (CT12 or CT13) increased it in SK-Hep1 cells. Consistently, MiaPaCa2 cells transfected with CT12 or CT13 exhibited a greater sensitivity to bortezomib. Evidence of G12/13’s antagonism on the anticancer effect of bortezomib was verified in the reversal by G12QL or G13QL of the minigenes’ enhancement of cytotoxity. Real-time polymerase chain reaction assay enabled us to identify PSMB5, multicatalytic endopeptidase complex-like-1, and proteasome activator subunit-1 repression by CT12 or CT13. Furthermore, G12/13 inhibition enhanced the ability of bortezomib to repress PSMB5, as shown by immunoblotting and proteasome activity assay. Moreover, this inhibitory effect on PSMB5 was attenuated by G12QL or G13QL. In conclusion, the inhibition of G12/13 activities may enhance the anticancer effect of bortezomib through PSMB5 repression, providing insight into the G12/13 pathway for the regulation of proteasomal activity.

  B. K Koo , K Waseda , H. J Kang , H. S Kim , C. W Nam , S. H Hur , J. S Kim , D Choi , Y Jang , J. Y Hahn , H. C Gwon , M. H Yoon , S. J Tahk , W. Y Chung , Y. S Cho , D. J Choi , T Hasegawa , T Kataoka , S. J Oh , Y Honda , P. J Fitzgerald and W. F. Fearon
 

Background— We sought to investigate the mechanism of geometric changes after main branch (MB) stent implantation and to identify the predictors of functionally significant "jailed" side branch (SB) lesions.

Methods and Results— Seventy-seven patients with bifurcation lesions were prospectively enrolled from 8 centers. MB intravascular ultrasound was performed before and after MB stent implantation, and fractional flow reserve was measured in the jailed SB. The vessel volume index of both the proximal and distal MB was increased after stent implantation. The plaque volume index decreased in the proximal MB (9.1±3.0 to 8.4±2.4 mm3/mm, P=0.001), implicating plaque shift, but not in the distal MB (5.4±1.8 to 5.3±1.7 mm3/mm, P=0.227), implicating carina shifting to account for the change in vessel size (N=56). The mean SB fractional flow reserve was 0.71±0.20 (N=68) and 43% of the lesions were functionally significant. Binary logistic-regression analysis revealed that preintervention % diameter stenosis of the SB (odds ratio=1.05; 95% CI, 1.01 to 1.09) and the MB minimum lumen diameter located distal to the SB ostium (odds ratio=3.86; 95% CI, 1.03 to 14.43) were independent predictors of functionally significant SB jailing. In patients with ≥75% stenosis and Thrombolysis In Myocardial Infarction grade 3 flow in the SB, no difference in poststent angiographic and intravascular ultrasound parameters was found between SB lesions with and without functional significance.

Conclusions— Both plaque shift from the MB and carina shift contribute to the creation/aggravation of an SB ostial lesion after MB stent implantation. Anatomic evaluation does not reliably predict the functional significance of a jailed SB stenosis.

Clinical Trial Registration: http://www.clinicaltrials.gov. Unique Identifier: NCT00553670.

 
 
 
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