One protein drives lung cancer spread: New study finds a way to block it

Tulane University researchers have discovered a previously undiscovered molecular route that could help to stop lung cancer in its tracks.

Lung cancer is the most frequent type of cancer and the main cause of cancer-related deaths worldwide. According to senior study author Dr. Hua Lu, the Reynolds and Ryan Families Chair in Translational Cancer at Tulane University School of Medicine, the research, published in Proceedings of the National Academy of Sciences, could lead to the development of a new anti-cancer drug and more personalized lung cancer treatment.

The researchers discovered that RBM10, a known tumor suppressor protein, can decrease lung cancer growth by reducing the action of c-Myc, a protein that, when overexpressed, causes cancer cell growth and proliferation. RBM10 collaborates with two ribosomal proteins (RPL5 and RPL11) to destabilize c-Myc and slow the progression of lung cancer, according to the findings.

These findings are the first to show that the proteins have an anti-cancer connection.

“We found that RBM10 can directly target c-Myc for degradation and reduce its cancer-causing effects by binding with RPL5 and RPL11,” he said. “We know a lot about cancer, but the molecules involved remain a mystery.” We are gradually obtaining a better grasp.”

Imagine two factories in a cell, each manufacturing parts for assembly into new protein machineries; c-Myc is a regular part of this protein production process—and cellular growth in general—and humans cannot live without it.

This manufacturing is occasionally disturbed, and firms begin creating defective parts. When cancer forms, it uses c-Myc to keep producing, allowing these “spare parts” to aggregate and create tumors. RBM10, in collaboration with RPL5 and RPL11, can destabilize c-Myc and inhibit tumor growth.

Importantly, the study demonstrated that a mutant form of RBM10 prevalent in lung tumors loses its ability to regulate c-Myc, fails to attach to the ribosomal proteins RPL5 and RPL11, and eventually promotes tumor growth rather than reducing it.

“RBM10 is an important protein that can suppress cancer cells, but when a cancer wants to develop, it will mutate RBM10 and block that function,” he said.

Lu intends to learn more about how the RBM10 mutant works in order to design an anti-cancer medicine that targets it.

“Hopefully we can design a molecule to specifically target the mutant, since that’s a special structure not existing in the normal tissue,” he said. “If we can convert this mutant, we can hopefully make it suppress c-Myc’s cancer-causing activity.”

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