As I am working on a project to study the role of TGF-Beta in prostate tumour progression (see more on an older post), everything TGF-Beta related catches my attention.
The Transforming Growth Factor Beta (or just TGFB) are a family of proteins that control cell proliferation and differentiation. I hope that my friends at Vanderbilt will correct me if they don’t agree with the statement that an imbalance in TGFB production and consumption could lead to uncontrolled growth and potentially to the beginning of a tumour.
Now, a group of researchers from New York and Barcelona led by Joan Massague have shown how TGFB plays also an important role by improving the chances of tumour cells originated in the breast to better to metastasise in the lung (although, curiously not in the bone). The research is reported in this week’s issue of Cell (as well as in the Spanish press for those of you that speak Spanish).
The research shows that TGFB allows cells to depart the primary tumour and empowers to disrupt the walls of capillaries in the lung vastly improving their chances of establishing a new tumour colony.
Thanks for the link – I’d somehow scanned the Cell table of contents without spotting this paper! It’s been added to my growing “to read” pile…
I have a good friend here @ Vandy who works on this stuff. I’ll point her to your blog to she what she thinks of that statement. I think there are several researchers here working on TGF-beta and prostate cancer.
This is what my friend had to say. “Ya, it sounds correct (I’m not sure exactly what he means by “consumption”,
but ya an imbalance of TGFß alters the homeostasis etc that can lead to
increased proliferation and contribute to tumor formation). Of course it may
depend on the cell getting further genetic alterations/ mutations.”
Cath: I know the feeling. My pile also keeps growing and it gets worse the more I read..
Nuruddeem: I know people at the Cancer Center working on the VUTMEN project, don’t know if those are the guys you know. Of course I agree that genetic alterations are probably a requirement for further tumour progression although the increased proliferation makes such an event more likely.
Clearly, the TGFB pathway can be tumor suppressive. In many tumor types TGFB is lost usually by epigenetic silencing of the receptor leading to increased proliferation. I don’t know of any evidence of TGFB serving as an tumor initiating oncogene (correct me if I’m wrong), however it clearly can play a major role in tumor progression and metastasis. One mechanism is through the induction of epithelial to mesenchymal transition and now this very interesting role of blood vessel permeability using ANGPTL4.
Thanks Jason, I also wonder how an excess of TGFB in the environment affects tumour progression. It might be not only that the TGFB pathway can be used by a tumour, by silencing it, but also that by producing more TGFB tumour cells could have a better chance ?