7
Views
4
CrossRef citations to date
0
Altmetric
Anatomical Pathology

Decreased expression of Bax-interacting factor-1 (Bif-1) in invasive urinary bladder and gallbladder cancers

, , , , , & show all
Pages 553-557 | Received 15 Sep 2007, Accepted 28 Nov 2007, Published online: 06 Jul 2009
 

Summary

Aims: Mounting evidence indicates that deregulation of apoptosis is involved in the mechanisms of cancer development. Bax-interacting factor-1 (Bif-1) interacts with both Bax and Bak that are crucial for the intrinsic apoptosis signalling. Functionally, loss of Bif-1 expression has been proven to enhance tumorigenesis. The aim of this study was to explore whether loss of Bif-1 expression occurs in urinary bladder (UB) and gallbladder (GB) cancer tissues.

Methods: We analysed Bif-1 protein expression in 41 transitional cell carcinomas of UB and 26 GB adenocarcinomas by immunohistochemistry.

Results: In both UB and GB, normal mucosal epithelial cells strongly expressed Bif-1 protein. In the UB cancers, Bif-1 expression was strongly positive in 25 cases (61.0%), but the remaining 16 cases showed no (14.6%) or markedly decreased (24.4%) Bif-1 immunostaining compared with the normal mucosal epithelial cells. Similarly, in the GB cancers, Bif-1 immunostaining was strong in 17 cases (65.4%), while the remaining nine cases showed no (15.4%) or markedly decreased (19.2%) Bif-1 immunostaining compared with the normal mucosal epithelial cells.

Conclusion: The decreased expression of Bif-1 in large fractions of both UB and GB cancers (39.0% and 34.6%, respectively) compared with their normal mucosal cells suggested that loss of Bif-1 expression might play a role in tumorigenesis in both UB and GB cancers, possibly by inhibiting apoptosis mediated by Bif-1.

Log in via your institution

Log in to Taylor & Francis Online

There are no offers available at the current time.

Related Research

People also read lists articles that other readers of this article have read.

Recommended articles lists articles that we recommend and is powered by our AI driven recommendation engine.

Cited by lists all citing articles based on Crossref citations.
Articles with the Crossref icon will open in a new tab.