Matk, also known as megakaryocyte-associated tyrosine kinase, and CHK in the context of CSK-homologous kinase, is involved in multiple biological functions.

In the context of bone metabolism, it plays a critical role in regulating the functions of osteoclasts and osteoblasts. In osteoclast precursor cells, Matk overexpression attenuates the formation of osteoclasts with actin rings, while knockdown enhances it. In osteoblasts, overexpression reduces bone nodule formation, and knockdown increases osteoblast function. Matk binds to Runx2, inhibiting its translocation into the nucleus and downregulating its target genes [1].

In colorectal cancer, the expression of CHK/MATK is significantly downregulated in CRC cell lines and primary tumours compared to normal colonic tissue. Promoter methylation is found to epigenetically silence CHK/MATK. Re-expression of CHK/MATK in CRC cell lines leads to reduced SFK activity, anchorage-independent growth, cell proliferation, migration in vitro, and tumour growth and metastasis in vivo, identifying it as a potential tumour suppressor gene [2].

In conclusion, Matk is crucial for bone metabolism and may serve as a tumour suppressor in colorectal cancer. Studies on Matk, especially through gene-manipulation models like overexpression and knockdown, have provided insights into its functions in these biological processes and disease conditions, potentially guiding future research in bone-related diseases and cancer treatment.