A Tulane University study has discovered a new way to stop lung cancer. It highlights RBM10's role in suppressing cancer growth and identifies a mutated form that promotes tumor growth, findings that could lead to the development of a new anti-cancer drug and more personalized treatments for lung cancer.
A new study from Tulane University has discovered a previously unknown molecular pathway that may help prevent the development of lung cancer.
Lung cancer is one of the most common cancers in the world and the leading cause of cancer-related death. The research, published in the Proceedings of the National Academy of Sciences, could lead to the development of a new anti-cancer drug and more personalized treatments for lung cancer, said Dr. Hua Lu, the study's senior author and the Reynolds and Ryan Family Chair in Translational Cancer at Tulane University School of Medicine.
The study found that a known tumor suppressor protein called RBM10 can inhibit the growth of lung cancer by inhibiting the function of c-Myc. The researchers found that RBM10 cooperates with two ribosomal proteins (RPL5 and RPL11) to destabilize c-Myc and hinder the spread of lung cancer. These findings identify, for the first time, a tumor-suppressive relationship between the two proteins.
"We found that RBM10 can directly target c-Myc for degradation and reduce its oncogenic effects by binding to RPL5 and RPL11," Lu said. "We know a lot about cancer, but the molecules involved are still a black box. We are deepening our understanding bit by bit."
To understand how this process halts the progression of lung cancer, imagine two factories in a cell, each making parts to assemble into new protein machines; c-Myc plays a regular role in this protein production process, as well as throughout cell growth, without which humans cannot survive.
Occasionally this production process is disrupted and the factory starts producing incorrect parts. When cancer begins to form, it uses c-Myc to continue production, allowing these "spare parts" to accumulate and form tumors. RBM10, with the help of RPL5 and RPL11, destabilizes c-Myc and prevents tumor growth.
Importantly, the study also found that a mutated form of RBM10 often found in lung cancer loses its ability to inhibit c-Myc and is unable to bind to the RPL5 and RPL11 ribosomal proteins, ultimately promoting tumor growth rather than inhibiting it.
"RBM10 is an important protein that suppresses cancer cells, but when cancer wants to develop, it mutates RBM10, blocking this function," Lu said.
The researchers hope to further study the function of the RBM10 mutant in the hope of developing anti-cancer drugs that target it. "Hopefully we can design a molecule that specifically targets the mutant, because this is a special structure that does not exist in normal tissue," Lu said. "If we can transform this mutant, we can hopefully make it inhibit the oncogenic activity of c-Myc."
Compiled from: ScitechDaily