Researchers have identified a protein that could slow the spread of lung cancer and lead to the development of new anti-cancer drugs.
Published in a new study, the research shows that a protein known to stop tumours called RBM10 can slow down the growth of lung cancer. It does this by hindering another protein called c-Myc, which usually makes cancer cells proliferate.
This is the first time that a connection hindering cancer has been identified with these proteins. The findings were published in the Proceedings of the National Academy of Sciences journal.
The team, from Tulane University in the US, found that RBM10 works with two other proteins (RPL5 and RPL11) to stop c-Myc and prevent lung cancer from spreading.
"We found that RBM10 can directly target c-Myc for degradation and reduce its cancer-causing effects by binding with RPL5 and RPL11," Dr Hua Lu, one of the study’s authors and a professor at Tulane University, 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".
Lung cancer is the second most commonly diagnosed form of cancer among men in Europe. An estimated 320,000 people in EU countries were expected to be newly diagnosed with it in 2020.
Current treatments involve surgery, chemotherapy, radiotherapy, and immunotherapy.
Targeting a key protein in cancer progression
C-Myc is a protein that is crucial in regulating cell growth and proliferation. Still, in the context of cancer, an overexpression or increased activity of c-Myc is often observed.
Myc deregulation plays a part in 70 per cent of human cancers, according to some estimates.
This overactive c-Myc can drive cancer cell growth, acting like a "gas pedal" for the cell cycle and promoting the uncontrolled reproduction of cells. This unregulated cell growth leads to the formation of tumours.
RBM10, assisted by RPL5 and RPL11, can disrupt c-Myc, halting cancer progression.
"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.
Crucially, the study revealed that a mutant version of RBM10, commonly identified in lung cancers, loses its capacity to inhibit c-Myc, supporting tumour growth rather than suppressing 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".