University of Illinois Cancer Center member Jing Liu, PhD, is the corresponding author on new work in the journal Cancer Letters that could point to potential therapies by highlighting the role of the protein Miz1 in KRAS oncogene-mutated non-small-cell lung cancer (NSCLC).
NSCLC is the most common lung cancer and KRAS is most often the mutated oncogene, according to the article.
“Our data suggest that oncogenic KRAS mutation induces upregulation of Miz1, which in turn promotes lung tumorigenesis through the repression of Pcdh10 [gene] expression,” wrote the authors, who included others from the University of Illinois Chicago. Among the authors is fellow Cancer Center member Xiaowei Wang, PhD, who like Liu is part of the Cancer Center’s Translational Oncology research program.
In a mouse model of KRAS-driven lung cancer, the authors showed that loss of function of Miz1 inhibits lung formation. In vitro, the silencing of Miz1 decreased cell proliferation and other functions while having little effect on normal cells. The Cancer Genome Atlas Lung Adenocarcinoma (TCGA-LUAD) database also indicated a connection of KRAS mutation to Miz1 in human NSCLC.