Researchers from Tulane University have uncovered a previously unknown molecular pathway that could be key to halting lung cancer. Their study in mice demonstrates that a known tumor suppressor protein called RBM10 can inhibit lung cancer growth by suppressing the function of c-Myc, a protein that drives cancer cell growth and proliferation when overexpressed. Researchers discovered that RBM10 partners with two ribosomal proteins (RPL5 and RPL11) to destabilize c-Myc and impede the spread of lung cancer.

Their findings are published in Proceedings of the National Academy of Sciences in an article titled, “RNA-binding motif protein 10 inactivates c-Myc by partnering with ribosomal proteins uL18 and uL5,” and led by senior study author Hua Lu, PhD, the Reynolds and Ryan Families chair in translational cancer at Tulane University School of Medicine.

These findings are the first to identify a cancer-inhibiting relationship between the proteins.

“We found that RBM10 can directly target c-Myc for degradation and reduce its cancer-causing effects by binding with RPL5 and RPL11,” Lu said. “We know a lot about cancer, but the molecules involved are still a black box. Piece by piece, we are gaining a better understanding.”

c-Myc plays a regular part in this protein production process—and cellular growth in general—and humans could not live without it. Occasionally, this process is disrupted. When cancer begins forming, it uses c-Myc to continue production, allowing these “spare parts” to accumulate and form tumors. RBM10, with the help of RPL5 and RPL11, can destabilize c-Myc and shut down tumor growth.

The research also discovered that a mutant form of RBM10 often found in lung cancers loses the ability to suppress c-Myc, fails to bind to the RPL5 and RPL11 ribosomal proteins, and eventually promotes tumor growth instead of suppressing 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,” Lu said.

Lu hopes to further study how the RBM10 mutant functions in the hope of developing an anticancer drug to target it.

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

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