New research is suggesting that the way stem cells talk to each other may partially explain why genes mutate and cause cancer. The study from Texas A & M looks at a class of proteins that communicate between cells called fibroblast growth factor (FGF). Mistakes in how FGF is transmitted and received by cells can activate previously dormant stem cells in an organ, which can cause cancer.
Fen Wang, director of the Texas A&M Center for Cancer and Stem Cell Biology, says:
“FGF is truly the Cinderella of cancer research. For decades it has been overlooked by big pharmaceutical companies because its role in cells is so complex. Now that we are starting to understand it, everyone is rushing to pay attention to the new star.”
The work by Wang and colleague Wallace McKeehan supports a previous theory in which cancer is a stem cell disease.
They have been studying how stem cells that cause cancer come out of dormancy and become active. If they can keep the cells dormant, they can ultimately prevent cancer from forming.
Stem Cells and Cancer Drugs
Stem cells have numerous different roles in human growth. Embryonic stem cells can become any cell or organ in the body.
However, each organ in the body also contains non-embryonic stem cells that are specific to that organ. These organ-specific stem cells control reproduction and growth of the organ through replenishing damaged or aged cells, as well as regeneration of tissues.
Researchers now believe that cancerous stem cells may set off reproduction and growth of cells within a cancer.
These cancerous stem cells hiding in the cancer, under the radar of cancer drugs that target cell proliferation, may underlie the relapse of tumors after surgery of the primary tumor or other cancer treatments. Moreover, without the cancer, stem cells cannot metastasize, or spread.
Some breast and prostate cancer cases have fueled the cancer stem cell theory.
Frequently years after the organ or the cancerous lesions are removed and the patient is declared cancer-free, breast or prostate cancer can return in other organs, indicating the cancer had metastasized before it was originally detected. Cancerous stem cells may be to blame.
What Is Normal?
Although almost all cells in the body expresses the FGF protein, there are 22 different types, so researchers have struggled to understand their role in cell communication. Until recently it has been unclear how one of the 22 different types of FGF were sent out by cell expressers and taken in by cell receivers.
The team traced the life cycle of multiple generations of cells to observe the normal pathways of FGF and what happens when a miscommunication occurs.
“This research is instrumental in establishing the way FGF is normally communicated in cells,” Wang says. “Before we can know what’s abnormal, we must first establish what is normal. It is particularly important to understand how FGF works in normal and cancerous stem cells.”
Wang and McKeehan’s research is specific to prostate stem cells and prostate cancer, but it could have implications for cancers in other organs as well.
“Current cancer therapies such as chemotherapy and radiation only target actively proliferating cancer cells,” Wang says. “If we can control how cancerous stem cells remain dormant and how they are activated, we can cure cancer. The research is still in the very early stages, but we have hope.”
Yanqing Huang, Tomoaki Hamana, Junchen Liu, Cong Wang, Lei An, Pan You, Julia Y. F. Chang, Jianming Xu, Wallace L. McKeehan and Fen Wang Prostate Sphere-forming Stem Cells Are Derived from the P63-expressing Basal Compartment The Journal of Biological Chemistry, 290, 17745-17752.
_Photo: Paul Andrews/Univ. Dundee, Wellcome Images _