A tumor-associated protein with cell-transforming properties has been identified as an attractive molecular target for the development of new therapies to prevent early-stage lung adenocarcinomas from progressing.

In a mouse model, the Rac1b protein stimulated a change in epithelial cells of the lung. The change, known as epithelial-mesenchymal transition (EMT), triggered tumor development and now appears to be a key step in lung cancer progression during the earliest stages of cancer, according to lead investigator and Mayo Clinic (Jacksonville, Florida) cancer biologist Derek Radisky, PhD.

Whereas normal cells recognize when they are dividing too rapidly and turn on programs that block inappropriate cell division, “here we found that early-stage lung cancer cells switch on EMT in order to bypass these controls,” Radisky explained in a Mayo Clinic statement describing the study findings, which were published in Science Translational Medicine (2012;4[142]:142ra95).

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EMT requires the ability of cells and tissues to morph from one type to another and develop in an orchestrated fashion. The process is a well-recognized transition in many types of late-stage solid tumors, which use EMT to change the tumor cells into a form that can migrate through the blood. This leads Radisky and colleagues to believe that the same early-stage use of EMT they discovered in lung cancer is likely occurring in other cancers as well. Inhibiting the function of the Rac1b protein, which is expressed abundantly in stage 1 and stage 2 lung adenocarcinomas, may represent a way to prevent progression of early-stage lung cancers.

“This study offers us great new clues for a new approach to treating lung and possibly other cancers as early as possible,” stated Radisky.