A group of researchers from the Institute of Molecular Genetics of the National Research Council (IGM-CNR) lead by Dr. Vittoria Cenni, in collaboration with Dr. William Blalock and funded by the Italian Association of Cancer Research (AIRC), has discovered that the proliferation as well as the clonogenic potential of cells from osteosarcoma, a malignancy primarily afflicting children and young adults, can be tempered by the abrogation of the expression of the mechanotransducer protein Ankrd2.
Before this study, the Ankrd2 protein was known for being mainly involved in muscle differentiation. In particular, in striated muscle cells, Ankrd2 acts as a transducer of mechanical and oxidative stimuli, transcriptionally modulating cell proliferation, differentiation and inflammation, thus participating in the adaptative response to stress.
Now, for the first time, this recent study demonstrates that Ankrd2 also plays a key role in tumor progression. In particular, it is not the overexpression, but rather the absence of Ankrd2 that has remarkable effects on the pathophysiology of osteosarcoma cells. The findings unequivocally prove that the absence of Ankrd2, obtained through the silencing of its mRNA, triggers a significant reduction of cellular proliferation, as well as of the tumor's clonogenic potential.

Modulating the expression of Ankrd2 and of its downstream effectors has the potential to open novel therapeutic avenue for the treatment and the cure osteosarcoma.

Piazzi M, Kojic S, Capanni C, Stamenkovic N, Bavelloni A, Marin O, Lattanzi G, Blalock W, Cenni V.
Ectopic Expression of Ankrd2 Affects Proliferation, Motility and Clonogenic Potential of Human Osteosarcoma Cells.
Cancers (Basel). 2021 Jan 6;13(2):174. doi: 10.3390/cancers13020174.
PMID: 33419058