Molecule Triggers Cell Death in Non-Small Cell Lung Cancer


A newly-discovered molecule can induce programmed cell death in mesenchymal-like lung cancer cells.

A single molecule may hold the key to fighting non-small cell lung cancer.

The molecule miR-124 plays a regulatory role that determines whether the cancer cells will experience programmed cell death, according to a study published by Science Signaling.

The molecule was found to induce programmed cell death among cancer cells that underwent epithelial to mesenchymal transformation. The mesenchymal-like cells have KRAS mutations and are usually resistant to traditional chemotherapy.

“Lung cancers display widespread genetic, molecular and phenotypic variability and heterogeneity,” said corresponding author Anurag Singh, PhD. “It is critical to understand the implications of this heterogeneity to identify effective targeted therapeutic regimens and clinical diagnostics.”

The American Cancer Society projects that there are 222,500 new cases of lung cancer each year in the United States, with non-small cell lung cancer accounting for up to 85% of cases, highlighting the need for new treatments.

In the study, the authors analyzed human lung cancer cells to characterize the profiles of 2 subtypes.

When looking at the biochemical profiles of the cells, the authors discovered miR-124 plays a significant role in the signaling cascade that determines whether the cell will live or die, according to the study.

These results suggest that miR-124 inhibitors may provide more effective treatment for patients with certain subtypes of non-small cell lung cancer.

The authors hope this finding will lead to clinical trials that treat patients with non-small cell lung cancer. They note that there must be additional work to investigate miR-124 as a cancer treatment.

“Understanding the mechanisms that are associated with phenotypic heterogeneity in lung cancer cells—specifically differences between epithelial and mesenchymal-like cells–allows these differences to be exploited to develop more selective therapeutic agents,” Dr Singh said.

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