KMID : 0358320070480050483
|
|
Korean Journal of Urology 2007 Volume.48 No. 5 p.483 ~ p.488
|
|
Analysis of the NF-¥êB and Apoptosis Inducing Genes in Bladder Tumor
|
|
Jung Pil-Du
Kim Yong-June Lee Sang-Cheol Kim Wun-Jae Yun Seok-Joong Han Kwang-Hee Lee Hyung-Lae
|
|
Abstract
|
|
|
Purpose: A multi-subunit transcription factor NF-¥êB mediates the antiapoptotic signals in several cancer cell lines and it is activated in a broad range of human tumors. In this study, we investigated whether the expression levels of the NF-¥êB and the apoptosis inducing genes were related to the pathogenesis and clinical properties of human bladder tumor.
Materials and Methods: The expressions of NF-¥êB, BCL2-associated X protein(BAX), BCL2-associated death protein(BAD) and BH3-interacting domain death agonist protein(BID) were investigated by performing immunohistochemical staining on 133 archival bladder tissue paraffin blocks; these blocks included 122 transitional cell carcinomas of the urinary bladder and 11 normal bladder mucosae.
Results: The expression levels of NF-¥êB were significantly higher in the bladder tumors than those of the normal bladder mucosae(p=0.001). The expression levels of BAX in the superficial and low-grade(grade 1 and 2) bladder tumors were significantly enhanced more than those of the high-grade and invasive cases(p=0.042 and p=0.045, respectively), while the expression levels of BAD in the tumor tissues and low-grade tumors were significantly elevated compared with those of the normal mucosae and high grade tumor(p=0.007 and p=0.048, respectively). But the expressions of BID were not correlated with any pathologic and clinical properties.
Conclusions: The expressions of the NF-¥êB and apoptosis inducing genes such as BAX and BAD are strongly associated with the pathogenesis and clinical properties of bladder tumor. (Korean J Urol 2007;48:483-488)
|
|
KEYWORD
|
|
NF-¥êB, BCL2-associated X protein, BCL2-associated death protein, BH3 interacting domain death agonist protein, Bladder tumor
|
|
FullTexts / Linksout information
|
|
|
|
Listed journal information
|
|
|