| Summary: | Objective: Cellular heterogeneity of tumors stems from cell populations expressing a unique set of proteins defective genetic and epigenetic networks. It is shown that versican (VCAN) is upregulated by transforming growth factor-beta (TGF-β1) in several types of cancer cell types. Our prior studies revealed that TGF-β1 expression is elevated in cancer stem cell (CSCs) monolayer cultures and VCAN expression was also significantly increased in spheroid formed CSCs.
Methods: Within the scope of these results, it was hypothesized that high TGF-β1 expression in the monolayer might trigger the three-dimensional architectural organization by inducing VCAN expression. This study investigated the expression profiling of VCAN in primary and secondary tumor-derived cell lines and the effect of TGF-β1 signaling in these cells.
Results: The findings showed that the VCAN gene expression level in the PC3 human prostate cell line was correlated with VCAN protein expression as analyzed by western blot. There was no inducing or suppressing effect of TGF-β1 on VCAN protein expression.
Conclusion: TGF-β1 has neither stimulatory nor inhibitory effects on VCAN expression in prostate cancer cells at the doses used in this study. In the metastatic, high VCAN protein levels were observed while no mRNA was detected which could have resulted from post-transcriptional changes such as increased protein stability and/or expression of different VCAN isoforms that may play an important role in the secondary tumor cells in prostate carcinoma.
|
|---|