Please use this identifier to cite or link to this item:
|Title:||The signalling pathway for BCG-induced interleukin-6 production in human bladder cancer cells|
|Authors:||Zhang, Y. |
Human bladder cancer cells
|Citation:||Zhang, Y., Yap, L.L., Khoo, H.E., Mahendran, R., Esuvaranathan, K. (2002). The signalling pathway for BCG-induced interleukin-6 production in human bladder cancer cells. Biochemical Pharmacology 63 (2) : 273-282. ScholarBank@NUS Repository. https://doi.org/10.1016/S0006-2952(01)00831-0|
|Abstract:||Intravesical bacillus Calmette-Guérin (BCG) is currently the therapy of choice for superficial bladder cancer with a 60-70% response rate. Induction of cytokine production (e.g. IL-6, etc.) by BCG has been found in patient's urine in vivo as well as bladder cancer cell lines. However, the signalling mechanisms are still unclear. In this study, we investigated the effect of BCG on cAMP production and its role in regulating interleukin-6 expression in the human bladder cancer cell line, MGH. After 1hr exposure to BCG, IL-6 gene expression in MGH cells increased by 2.5-3-fold and cAMP production increased by 8-10-fold in a time- and dose-dependent manner. BCG-induced cAMP production was inhibited by both antifibronectin antibody and an adenylate cyclase inhibitor, SQ22536 in a dose-dependent way. In the presence of SQ22536, IL-6 expression in MGH cells was also greatly reduced. Furthermore, cAMP-dependent kinase inhibitors H7 and HA1004 also inhibited BCG-induced IL-6 expression in MGH, with HA1004 being much less effective than H7. Thus, BCG induces cAMP production and may regulate interleukin-6 expression partially via a cAMP-dependent pathway in human bladder cancer cells. © 2002 Elsevier Science Inc. All rights reserved.|
|Source Title:||Biochemical Pharmacology|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Feb 14, 2019
WEB OF SCIENCETM
checked on Jan 29, 2019
checked on Feb 9, 2019
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.