Scientists may have figured out a brand new way to treat lung cancer by using a protein that inhibits tumor growth.
This previously unknown molecule pathway could help researchers develop personalized lung cancer treatments, a new study in the journal Proceedings of the National Academy of Sciences (PNAS) reveals.
The researchers found that a protein called RBM10—previously known to be a tumor suppressor—can inhibit the growth of lung cancer by stopping the function of another protein called c-Myc. c-Myc drives cancer cell growth when it is overexpressed in the body.
In the study, the scientists describe how they used RBM10 to partner with two other proteins, RPL5 and RPL11, to destabilize c-Myc and prevent the proliferation of lung cancers.
“We found that RBM10 can directly target c-Myc for degradation and reduce its cancer-causing effects by binding with RPL5 and RPL11,” study co-author Hua Lu, the Reynolds and Ryan Families Chair in Translational Cancer at the Tulane University School of Medicine, said in a statement. “We know a lot about cancer, but the molecules involved are still a black box. Piece by piece, we are gaining a better understanding.”
Proteins are made in the cell by little organelles called ribosomes, which read the code of our DNA—after being transcripted into mRNA—and translate it into proteins. Cancers can occur when the DNA being read is mutated, causing the cell to grow and reproduce uncontrollably. The c-Myc protein encourages cancer growth due to its role in the protein production process, as it allows proteins to carry on being produced despite a cancerous mutation, forming tumors.
“c-Myc is essential for the growth and proliferation as well as drug resistance of cancer and cancer stem cells. These functions are primarily attributed to c-Myc’s transcriptional regulation of 10 to 15 percent of the genome, including proteins, both ribosomal and nonribosomal, and noncoding, regulatory RNAs,” the authors wrote in the paper. “Controlling c-Myc expression and activity is critical for preventing cancer cell growth, proliferation, and drug resistance”
The scientists found that RBM10, with the help of RPL5 and RPL11, can destabilize c-Myc and therefore prevent it from boosting cancer growth. They also found that in lung cancers, there is often a mutant form of RBM10 that no longer suppresses c-Myc and cannot bind to RPL5 and RPL11, therefore promoting tumors rather than suppressing them.
“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.
The researchers hope to use these findings of RBM10’s functions and role in cancer suppression to develop drugs to treat lung cancer by targeting RBM10 itself.
“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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