NDLI: The DNA damaging agent VP16 induces the expression of a subset of ligands from the EGF system in bladder cancer cells, whereas none of the four EGF receptors are induced

Content Provider	Springer Nature Link
Author	Sørensen, Boe Sandahl Tørring, Niels Bor, Mustafa Vakur Nexø, Ebba
Copyright Year	2004
Abstract	Increased activity of the EGF system exerts a cell survival function in the presence of cytotoxic agents. The aim of our investigation was to identify the ligands and receptors from the EGF system, that are induced by the chemotherapeutic DNA damaging agent VP16 in bladder cancer cell lines. By use of real-time RT-PCR assays for all four receptors and six ligands from the EGF system we demonstrate that in HCV29 bladder cancer cells, amphiregulin, HB-EGF, and epiregulin mRNA levels are elevated (more than 100, 5, and 4 fold, respectively) by VP16. The remaining ligands (EGF, TGFα and betacellulin) are uninduced. The same was found for T24A bladder cancer cells, except that TGFα also was induced. The four receptors were reduced by VP16 in both cell lines. This demonstrates that the induction of the EGF system is mediated by an increased expression of a subset of the ligands, whereas the four receptors are reduced. For amphiregulin and HER1 we investigated with ELISA assays if the effects of VP16 also were observed at the protein level. We found that VP16 increase the amount of amphiregulin peptide both in the cell membrane and the culture medium. Similarly, the reduced EGF receptor mRNA expression correlated with reduced HER1 protein.Several investigations have shown that labile protein factors can be involved in the regulation of stress inducible growth factors and cytokines. We investigated if a labile protein regulates the expression of the subset of ligands that were induced with VP16. Blocking of protein neosynthesis with cycloheximide resulted in induced mRNA expression of exactly the same subset of ligands as observed with VP16 treatment of both HCV29 and T24A cells. This suggests that a labile protein factor regulates either the transcription or degradation of these mRNA's, and it can be speculated that VP16 also operate by inhibiting the activity of this factor. This is further stressed by the observation that combined treatment with cycloheximide and VP16 show no additive effect.In conclusion, we show that a subset of ligands from the EGF system is upregulated by VP16, whereas none of the four receptors are induced. This might represent a physiological response aimed at rescuing the cells.
Starting Page	129
Ending Page	135
Page Count	7
File Format	PDF
ISSN	03008177
Journal	Molecular and Cellular Biochemistry
Volume Number	260
Issue Number	1
e-ISSN	15734919
Language	English
Publisher	Kluwer Academic Publishers
Publisher Date	2004-01-01
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Cardiology Medical Biochemistry Oncology Biochemistry
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine Clinical Biochemistry Molecular Biology

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